Orthostatic Hypertension: When Pressor Reflexes Overcompensate

Joshua Fessel; David Robertson


Nat Clin Pract Nephrol. 2006;2(8):424-431. 

In This Article

Orthostatic Hypertension-definition and Significance

Orthostatic hypertension is an underappreciated but potentially clinically important entity. As alluded to above, orthostatic hypertension is defined simply as an increase in blood pressure upon assumption of upright posture. One problem with the literature on this subject is that very few studies have entailed direct measurement of arterial blood pressure in people with orthostatic hypertension. Such measurements would more faithfully reflect intra-arterial pressure and would avoid the introduction of potential artifacts associated with noninvasive blood pressure monitoring (e.g. improper cuff size, incompressibility of atherosclerotic arteries, and the effect of the time required physically to make the measurement). In addition, sphygmomanometers can underestimate blood pressure when it is perturbed by pressor reflexes, such as those engaged by upright posture, or if it is increased by pressor agents.[16] Therefore, the magnitude of the blood pressure increase upon standing might be even larger than is generally reported in orthostatic hypertensive subjects.

The magnitude of increase in sphygmomanometric pressure required for a diagnosis of orthostatic hypertension has often been operationally defined in individual studies, with an increase in SBP of 20 mmHg or more being a common recent diagnostic criterion (Box 1). Recognition of the presence and degree of orthostatic hypertension might be clinically important for a number of reasons. First, orthostatic hypertension might be a symptom of another treatable condition, such as pheochromocytoma[17,18] or mast-cell activation disorder in the context of POTS.[19] Second, orthostatic hypertension resulting from any number of causes might be an important risk factor for silent cerebrovascular ischemia and infarct. Published studies from the Shimada laboratory indicate that, at least in populations of elderly Japanese people with essential hypertension, the incidence of silent cerebrovascular infarct detectable by MRI is higher in those patients who have clinically identifiable orthostatic hypertension.[20,21]

Although other operational definitions of orthostatic hypertension have been used in various studies, the systolic blood pressure criterion above forms the basis of discussion in this Review as it has been associated with an important clinical condition—silent cerebrovascular ischemia.

Orthostatic hypertension has been a recognized phenomenon for quite some time. Some of the earliest reports discussing orthostatic hypertension were written by David HP Streeten in the 1970s and 1980s. The phenomenon was characterized as a DBP above 90 mmHg plus a greater increase in DBP upon standing than that experienced by hypertensives without orthostatic hypertension or by normotensives.[22] Those individuals with orthostatic hypertension also had a greater decrease in cardiac output, greater venous pooling in the lower extremities, and higher plasma norepinephrine levels upon standing. The hypothesis was that excessive venous pooling led to a decrease in cardiac output, the response to which was increased sympathetic activity and increased DBP. Streeten also commented that orthostatic hypertension was probably more common than was generally appreciated, but little or no mention was made of the possible clinical significance of the phenomenon.


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