Stages of Hypertension
Monday, Dec 10 2007
As physicians of the twentieth century began to employ newly developed measurement strategies for assessing blood pressure as part of patient evaluations, it became clear that interpretive parameters or guidelines were needed to determine risk for diseases associated with specific blood pressure values.
Although truly elevated or remarkably low blood pressures were an obvious concern for physicians of the early twentieth century, there was no general agreement regarding when a specific blood pressure might place a given patient at risk for developing problems of blood circulation.
The medical community needed to await the results of epidemiologic research conducted in the 1960s that clearly delineated the risk associated with various levels of blood pressure. Based upon these epidemiological findings, physicians adopted 160 mm Hg SBP and 100 mm Hg DBP as cut-off values for exhibiting increased risk for cardiovascular disease that warranted medical intervention, values that continue to be used today.
Beginning in 1977, the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health regularly assembled groups of experts from their own laboratories as well as from a number of professional and voluntary organizations to review the body of evidence to date and make recommendations regarding the detection, evaluation, and treatment of high blood pressure. Each of these joint national committees (JNC) has disseminated the conclusions of its review to the scientific community and the public through a report, the most recent being released in December 2003 (Chobanian et al., 2003).
It is well beyond the scope of this site to describe the various changes in recommendations that have occurred over the past several decades. Therefore, only the description of stages of hypertension from the most recent versions of the reports (JNC-6 and JNC-7) will be presented here (see Table 1.1).
As with preceding JNC reports, there were significant changes in the classification system from JNC-6 to JNC-7. Note that the upper two stages of hypertension severity in JNC-6 were combined in JNC-7, suggesting that the most recent data did not support separating these two levels of severity with respect to recommended interventions. The commonly used term ‘borderline essential hypertension,’ which had typically referred to mildly elevated blood pressures in the 140вЂ“160 mm Hg SBP or 90вЂ“95 mm Hg DBP range (Julius and Hannsson,1983), has been subsumed into the categorization as Stage 1 hypertension in the most recent versions of the JNC diagnostic guidelines.
Even more interesting is the fact that the two levels that JNC-7 labeled ‘normal’ and ‘high normal’ were renamed ‘pre-hypertensive.’ This is a significant change that has aroused considerable debate among researchers and clinicians who specialize in working with essential hypertensive patients.
The use of the pre-hypertensive category was based on recent data showing that individuals in this category had a 90 percent greater risk of developing hypertension than persons with lower blood pressures (Vasan et al., 2002) and that risk for cardiovascular mortality among persons in this category increases for every 20 mm Hg above a SBP of 115 mm Hg or for every 10mm Hg above a DBP of 75mm Hg (Lewington et al., 2002).
Mancia (2003) objected to the use of the term ‘pre-hypertensive’ on the basis that physicians do not diagnose normal patients as pre-diseased and that many so-called ‘prehypertensive’ patients may become unnecessarily worried about their current health condition.
He also claimed that the data supported intervention for patients in this group only if there was evidence of additional risk factors for cardiovascular disease. Mancia advocated the continued use of the JNC-6classification system, which is more consistent with the classification system initially developed by the International Society of Hypertension (ISH) and the World Health Organization (WHO) and recently adopted in Europe (Guidelines Committee, 2003). There is, of course, continuing controversy regarding the specific criteria that physicians should apply in making diagnoses and developing effective intervention plans for their hypertensive and prehypertensive patients.
There has also been disagreement regarding whether elevations in systolic or diastolic blood pressures were associated with greater risk.
For decades, physicians had focused primarily on diagnosing hypertension on the basis of casual DBP. However, findings from the Framingham Study have indicated that increased SBP may pose a greater health risk than increased DBP (Kannel, Gordon, and Schwartz, 1971; Lloyd-Jones et al., 1999). This is particularly important among older adults, who often exhibit what has been termed isolated systolic hypertension. Among older adults, it has been documented that SBP continues to increase with aging, while DBP tends to plateau around the age of 60(Franklin et al., 1997). Older adults with isolated systolic hypertension are characterized by SBPs in the hypertensive range accompanied by normal DBPs. Pulse pressure, calculated as the difference between SBP and DBP, is elevated among these patients, as is their risk for cardiovascular complications (Domanski et al., 1999; Psaty et al., 1992). According to the JNC-7guidelines, DBP is a better predictor of cardiovascular risk until the age of 50, and SBP is a better predictor of cardiovascular risk thereafter.
Regardless of the exact criteria used in JNC guidelines and the ongoing discussions regarding when to treat or not to treat elevated blood pressure, all agree that the higher one’s blood pressure is, the more risk for cardiovascular disease and stroke increases. Blood pressure, after all, is a continuous variable that constantly adjusts to current physiological or environmental demands.
It really may not be that important to quibble over whether a patient with a blood pressure of 138/88 mm Hg should be categorized as a pre-hypertensive patient or fall into the high normal category; rather, it may be more important to inform him or her where his or her blood pressure falls with regard to the normal distribution of blood pressure and what efforts he or she might put into place to reduce it.
Modern medicine often has dichotomized continuous variables in an effort to develop decision rules that can be used to conform to a medical diagnosis and respond to a proscriptive treatment. As such, a hypertensive patient with a blood pressure of 140/90mm Hg is often treated much more like a patient with a blood pressure of 158/99 mm Hg than a patient with a blood pressure of 138/88 mm Hg. Despite our inclination to dichotomize blood pressures into the various stages described above, it is probably best to remember that blood pressure is a continuous variable and that risk for cardiovascular disease increases as blood pressure increases.
Development of essential hypertension appears to progress through different stages characterized by distinct physiological profiles. Early hypertension, or what had previously been termed ‘borderline’ essential hypertension, is characterized by mildly elevated blood pressures that typically are quite variable and often do not show a chronic progression to more elevated blood pressures over time.
Certainly, some ‘borderline’ essential hypertensive patients go on to develop sustained elevations in arterial pressure, but the majority do not (Julius, Weder, and Egan, 1983). Pathophysiologically, ‘borderline’ essential hypertensive patients have been shown to exhibit enhanced beta-adrenergic responsiveness, which leads to increased heart rate and increased blood volume ejected from the heart.
These findings led to the characterization of this group of patients as neurogenic in origin and exhibiting ‘hyperkinetic’ circulation (Julius and Esler, 1975). It should be noted that not all ‘borderline’ essential hypertensives fit this profile, but the hyperkinetic state is much more likely to be observed among ‘borderline’ hypertensives than among patients with sustained elevated blood pressures. In contrast, sustained hypertensive patients tend to exhibit normal or decreased cardiac action accompanied by increased vascular resistance to blood flow.
In brief, blood pressure elevations of ‘borderline’ essential hypertensive patients are more closely associated with increases in cardiac output, while blood pressure elevations of sustained hypertensive patients are more closely linked to increases in total peripheral resistance.
Although the differentiation between hypertension resulting from increased cardiac output (hyperkinetic hypertension) and hypertension resulting from altered vascular resistance has been observed consistently, it was unclear whether the two groups represented distinct categories of elevated blood pressure profiles or whether patients progressed from hyperkinetic hypertension to vascular-resistance hypertension as they aged.
To examine this question, prospective data were needed in which hyperkinetic hypertensive patients were followed over time. Lund-Johansen (1991) conducted such a study in which a group of hyperkinetic hypertensive patients were followed over 20 years. At the beginning of the study, young hypertensive patients had higher blood pressures associated with higher cardiac outputs, but measures of total peripheral resistance comparable to normotensive volunteers.
At 10- and 20-year follow-up assessments, the elevated blood pressures among hypertensive patients shifted from the original hyperkinetic hemodynamic profile to a profile characterized by low cardiac output and elevated total peripheral resistance. Interestingly, this progression from cardiac-related to vascular-related hypertension also occurred among hypertensive patients who had achieved good blood pressure control with anti-hypertensive medication. The same transition from cardiac-related to vascular-related hypertension has been observed in experimental animal models of hypertension (Guyton, 1992).
Semenchuk, E. M., and Larkin, K. T.
Published with assistance from the foundation established in memory of Amasa Stone Mather of the Class of 1907, Yale College.
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Last revised: by Dr. J. Gregory Frits, , M.D.
Provided by Armina Hypertension Association
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