Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Published Online
on May 13, 2002

Circulation. 2002
Published online before print May 13, 2002, doi: 10.1161/01.CIR.0000017186.52382.F4
A more recent version of this article appeared on May 28, 2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
105/21/2518    most recent
01.CIR.0000017186.52382.F4v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ketch, T.
Right arrow Articles by Robertson, D.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Ketch, T.
Right arrow Articles by Robertson, D.
Related Collections
Right arrow Other hypertension
Right arrow Other etiology
Right arrow Other Treatment
Right arrow Other Vascular biology

Submitted on January 29, 2002
Revised on March 20, 2002
Accepted on March 21, 2002

Four Faces of Baroreflex Failure. Hypertensive Crisis, Volatile Hypertension, Orthostatic Tachycardia, and Malignant Vagotonia

Terry Ketch MD, Italo Biaggioni MD, RoseMarie Robertson MD, and David Robertson MD*

From the Autonomic Dysfunction Center, Vanderbilt University, Nashville, Tenn.

* To whom correspondence should be addressed. E-mail: david.robertson{at}mcmail.vanderbilt.edu.

Background—The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences.

Methods and Results—Impairment of the baroreflex may produce an unusually broad spectrum of clinical presentations; with acute baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest.

Conclusions—Although baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of baroreflex failure requires specific strategies, which may lead to successful control.


Key words: baroreceptors • hypertension • tachycardia