Orthostatic Hypertension: When Pressor Reflexes Overcompensate

Joshua Fessel; David Robertson

Disclosures

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

In This Article

Diagnosis and Treatment

Fortunately, although orthostatic hypertension is an underappreciated clinical phenomenon, diagnosis of the condition is relatively straightforward. What is lacking in terms of diagnosis, however, is a standardized value for the increase in SBP and/or DBP to make the diagnosis of orthostatic hypertension. The criteria used in the study by Kario et al. that linked orthostatic hypertension to an increased incidence of silent cerebrovascular disease defined orthostatic hypertension as a ≥20 mmHg increase in SBP upon assumption of an upright posture (specifically in the study, head-up tilting to 70 degrees) from the supine position.[21] This definition, in the absence of other more rigorous diagnostic criteria, seems an appropriate definition to use, as this is a diagnostic criterion that has been associated with a clinically relevant endpoint. Although different studies have varied in their use of either passive tilting or active standing to elicit orthostatic hypertension, the phenomenon and associated clinical findings are seen with passive tilting[21] and active standing.[25] Evaluation of any patient in either the setting of a health maintenance visit or the setting of a work-up for a blood pressure abnormality should include measurement of blood pressure in the supine, sitting, and standing positions. A problem that arises immediately with the current state of knowledge is what the next step should be for a patient who is found to have orthostatic hypertension. Certainly the phenomenon should be considered a real finding if a patient shows an increase of ≥20 mmHg SBP upon standing from a supine position on more than one occasion. A demonstration of reproducibility is important for any orthostatic blood pressure changes, as patients with underlying blood pressure dysregulation (e.g. essential hypertension) and/or comorbidities that can impact upon blood pressure (e.g. diabetes mellitus) may well have more variable blood pressure readings than otherwise healthy normotensive subjects. The indications for further work-up should be based upon other findings independent of the orthostatic hypertension itself. For example, if a patient is found to have labile hypertension that is refractory to aggressive therapy, a diagnostic work-up for baroreflex failure and/or a search for surgically correctable causes of hypertension should be undertaken. Currently there is not sufficient data to suggest expensive or invasive testing for patients who are either normotensive or essentially hypertensive who also have asymptomatic orthostatic hypertension.

Therapeutic considerations are currently as challenging as recommendations for diagnostic measures. Treatment should primarily be guided by the condition that is the context for the orthostatic hypertension. For example, treatment for a patient with essential hypertension who has a component of asymptomatic orthostatic hypertension should be geared toward achieving optimal blood pressure control as for any patient with essential hypertension. The sum of the existing data would suggest that therapy targeted at controlling orthostatic hypertension would be aimed at controlling the effects of sympathetic activation. This could include therapies such as alpha-1 adrenergic receptor antagonists such as prazosin, used in the study by Raffia et al., or central alpha-2 adrenergic receptor agonists such as clonidine. There are currently no data to indicate whether orthostatic hypertension should be specifically targeted therapeutically, which therapy would be optimal, or what the therapeutic endpoints would be.

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