michigan hypertension core curriculum - State of Michigan

orthostatic hypotension, especially in elderly patients, is the risk of serious injury due to falling due to
syncope or near-syncope, with resulting hip fracture or head injury. The severe supine hypertension
that frequently accompanies OH is also a potential source of morbidity. All elderly patients and all
patients at increased risk of OH including those with diabetes mellitus and those with neurologic
diseases should be screened for orthostatic decreases in BP. Ambulatory 24 hour BP monitoring may
be helping in detecting or monitoring the supine hypertension associated with this syndrome.
Shibao 2 reported that hospitalizations in patients with OH numbered 233 per 100,000 in
patients over 75 years old, with a median length of hospital stay of three days, and an in-hospital
mortality rate of 0.9%. Equally discomforting is the observation of increased mortality in patients with
OH. Middle aged patients with OH in the Atherosclerosis Risk in Communities Study experienced a
hazard ratio of death of 2.0 (95% CI 1.6-2.7) 3 even after adjustment for known cardiovascular risk
factors or after excluding those dying with the first 2 years of follow-up and those with known cancer,
diabetes, CHD, hypertension and CVA. Elderly patients with OH also have increased mortality. 4
Pathophysiology and Etiology
The physiology of the baroreflex is complex (figure 1). Baroreceptors are stretch sensitive receptors
located in the adventitia of blood vessels. The major function of the baroreflex appears to be short term
regulation of BP and buffering of minute to minute blood pressure fluctuations. The term “receptor”
is a misnomer as BRs work by relaying afferent signals to the brainstem, not by receptor mediated
signaling. The most sensitive BRs are located in the aortic arch and sinuses of the left and right carotid
arteries, but other receptors are situated in the inferior vena cava and heart. The innervation of the
carotid sinus and aortic arch BRs are through the glossopharyngeal nerve (CN IX) and the vagus
nerve (CN X) respectively. Increases in BP result in stretching of blood vessel walls and generation of
action potentials within BRs. This effect is enhanced with higher elevations in BP. Generated action
potentials travel to the nucleus of the solitary tract located in the medulla. Here, glutaminergic excitatory
fibers activate the caudal venterolateral medulla which in turn sends inhibitory GABAnergic signals to
the rostral venterolateral medulla (RVML). This inhibition results in parasympathetic stimulation with a
resultant reduction in heart rate and a drop in peripheral resistance and thus lowering blood pressure.
Conversely, a reduction in BP as seen in low output states, results in decreased baroreceptor firing and
inhibits parasympathetic vagal response, which activates the RVML causing sympathetic activation
(increased cardiac output, systemic venous return and total peripheral resistance) and an increase in
NKFM & MDCH 217