(Circulation. 1997;96:575-580.)
© 1997 American Heart Association, Inc.
Articles |
Effects of Volume Loading and Pressor Agents in Idiopathic Orthostatic Tachycardia
From the Clinical Research Center, Departments of Medicine (G.J., J.R.S., B.B., I.B., R.M.-G., R.M.R., D.R.), Pharmacology (G.J., J.R.S., I.B., R.M.-G., R.M.R., D.R.), and Neurology (D.R.), Vanderbilt University Medical Center, Nashville, Tenn.
Correspondence to David Robertson, MD, Clinical Research Center, AA3228 MCN, Vanderbilt University, Nashville, TN 37232-2195. E-mail david.robertson{at}mcmail.vanderbilt.edu
Background Idiopathic orthostatic
tachycardia (IOT) is characterized by an increase in heart
rate (HR) with standing of 
30 bpm that is associated with elevated
catecholamine levels and orthostatic symptoms.
A dynamic orthostatic hypovolemia and
1-adrenoreceptor hypersensitivity have
been demonstrated in IOT patients. There is evidence of an autonomic
neuropathy affecting the lower-extremity blood vessels.
Methods and Results We studied the effects of
placebo, the 1-adrenoreceptor agonist
midodrine (5 to 10 mg), the
2-adrenoreceptor agonist clonidine (0.1
mg), and IV saline (1 L) in 13 patients with IOT. Supine and upright
blood pressure (BP) and HR were measured before and at 1 and 2 hours
after intervention. Midodrine decreased both supine and upright HR (all
HR values are given as bpm) at 2 hours (from 78±2 supine to 108±5
upright before treatment and from 69±2 supine to 95±5 upright after
treatment, P<.005 for supine and P<.01 for
upright). Saline decreased both supine and upright HR (from 80±3
supine to 112±5 upright before infusion and from 77±3 supine to 91±3
upright 1 hour after infusion, P<.005 for supine and
P<.001 for upright). Clonidine decreased supine HR (from
78±2 to 74±2, P<.03) but did not affect the HR increase
with standing. Clonidine very significantly decreased supine
systolic BP (from 109±3 at baseline to 99±2 mm Hg at 2
hours, P<.001), and midodrine decreased supine
systolic BP mildly.
Conclusions IOT responds best acutely to saline
infusion to correct the underlying hypovolemia. Chronically, this can
be accomplished with increased salt and water intake in conjunction
with fludrocortisone. The response of patients to the
1-agonist midodrine supports the hypothesis of partial
dysautonomia and indicates that the use of 1-agonists to
pharmacologically replace lower-extremity postganglionic sympathetics
is an appropriate overall goal of therapy. These findings are
consistent with our hypothesis that the tachycardia
and elevated catecholamine levels associated with IOT are
principally due to hypovolemia and loss of adequate lower-extremity
vascular tone.
Key Words: tachycardia • syncope • blood volume • blood pressure • catecholamines
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