Syncope and Orthostatic Hypotension DAVID ATKINS, M.D., BARBARA HANUSA, Ph.D., TERRY SEFCIK, M.s., WISHWAKAPOOR, M.D., M.P.H., Pittsburgh, Pennsylvania

PURPCSE: The purpose of this study was to de- termine the postural blood pressure response over time, the prevalence of orthostatic hypoten- sion in patients with syncope, and the relation- ship of orthostatic hypotension to recurrence of symptoms.

PATIENTS AND METHODS: we prospectively evaluated 223 patients with syncope in a stan-

. dardued manner. Orthostatic responses were measured in a standardized fashion at 0, 1,2,3,5, and 10 minutes or until symptoms occurred. Fol- low-up was obtained at 3-month intervals. Causes of syncope were assigned by predeter- mined criteria.

RESULT& Orthostatic hypotension (20 mm Hg or greater systolic blood pressure decline) was found in 69 patients (31%). The median time to reach minimal standing systolic blood pressure was 1 minute for all subjects. In patients with orthostatic hypotension (20 mm Hg or greater), meanthnetoreach minimum blood pressure was 2.4 minutes. The vast majority of patients with significant orthostatic hypotension had this fmding within 2 minutes of standing. Orthostatic hypotension was common in patients for whom other probable causes of syncope were assigned. The recurrence of syncope was not related to the degree of orthostatic hypotensiom however, the recurrence of dizziness and syncope as end- points was lower in patients with 20 mm Hg or greater systolic blood pressure reductions as compared with patients with lesser degrees of orthostatic blood pressure declines.

CONCLUSION: Orthostatic hypotension is com- mon in patients with syncope and is detected in the vast majority of patients by 2 minutes. Al- though symptom recurrence on follow-up was

From the Department of Medicine, University of Pittsburgh, Pitts- burgh, Pennsylvania.

This study was supported in part by grants from the Richard King Mellon Family Foundation and the National Heart, Lung, and Blood Insti- tute (ROl HL36735). Dr. Kapoor is a recipient of a Research Career Development Award from the National Heart, Lung, and Blood Institute (K04L 01899).

Requests for reprints should be addressed to Wishwa Kapoor, M.D., M.P.H., Room 100 Lothrop Hall, 190 Lothrop Street, Pittsburgh, Penn- sylvania 15261.

Dr. Atkins’ current affiliation: University of Washington, Seattle, Washington.

Manuscript submitted November 29, 1990, and accepted in revised form April 26, 1991.

lower in patients with more severe orthostatic hypotension, the clinical significance of this fmding needs to be further defined by future studies.

R ecent studies of syncope have identified ortho- static hypotension as the primary cause in 4%

to 9% of adults [l-6] and 20% of children [7] evalu- ated for loss of consciousness. Although orthostatic hypotension is an important cause of syncope, sev- eral issues regarding orthostasis and loss of con- sciousness have not been clarified.

First, recommendations vary on which parameter (systolic, diastolic, or mean blood pressure) is the best measure of orthostasis [3-lo], how long pa- tients should stand before blood pressure is mea- sured [11-E], and what defines a significant change in blood pressure [9,13,14].

Second, establishing that orthostatic hypoten- sion caused a p,articular episode of syncope is often problematic. Previous studies of syncope identified only those patients with symptomatic or extreme changes in blood pressure in whom there was no other evident cause of syncope [l-6]. However, as noted by Lipsitz [15], multiple disorders may act synergistically to cause syncope, especially in the elderly. It is possible that even moderate orthosta- sis contributed to syncope in some patients who had other identifiable causes of syncope.

Third, the importance of an abnormal but a- symptomatic decrease in blood pressure is contro- versial. While blood pressure in young, healthy sub- jects changes minimally upon standing, substantial declines in systolic blood pressure are common in the elderly [11,16-191. Although rarely accompa- nied by symptoms, a reduction of 20 mm Hg or more in standing systolic pressure has been associated with an increased risk of falls in the elderly [20], syncope in the institutionalized elderly [21], and death in hypertensive patients [22]. The relation- ship of orthostatic hypotension to clinical outcomes (e.g., recurrent syncope, presyncopal symptoms, or death) in patients who have had syncope has not been previously studied.

To address these issues, we conducted a prospec- tive study of syncope patients with the following aims: (1) To describe the timing of postural changes in blood pressure during prolonged standing (for 10

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SYNCOPE AND ORTHOSTATIC HYPOTENSION / ATKINS ET AL

minutes) in syncope patients. (2) To examine the prevalence of orthostatic hypotension in patients with and without other documented causes of syn- cope. (3) To examine the importance of orthostatic hypotension as a risk factor for recurrence of synco- pal or presyncopal symptoms. (4) To describe fea- tures of those patients in whom orthostatic hypo- tension was a probable cause of syncope.

ing standing, a final measurement was repeated and the test was terminated if the patient was unable to continue standing.

PATIENTS AND METHODS Syncope was defined as a sudden, transient loss

of consciousness associated with an inability to maintain postural tone that was not compatible with a seizure disorder, vertigo, dizziness, coma, shock, or other states of altered consciousness. Pa- tients who required pharmacologic or electrical car- dioversion at their initial presentation were not included.

Orthostatic change in blood pressure was calcu- lated as the difference between the supine and standing value for each time point. The maximal value for orthostatic change for each patient was used for further analysis. Immediately on presenta- tion, a small number of patients were evaluated after therapy (fluid or blood replacement) that was likely to have altered orthostatic findings. For this group, we compared our measures of orthostatic hypotension with those recorded by the emergency room physician, and used the greater value.

Follow-Up

Patient Accrual Patients were accrued from the emergency room,

inpatient wards, and outpatient clinics of the Pres- byterian-university Hospital from August 1987 to September 1989. All adult patients (age 16 years or greater) entered in this study underwent a stan- dardized evaluation after presenting with syncope to our medical center. The evaluation consisted of (1) a complete history and physical and neurologic examination; (2) baseline laboratory testing; (3) 12- lead electrocardiogram; (4) prolonged electrocar- diographic monitoring by ambulatory monitoring or by bedside monitoring in a telemetry unit except that it was optional in outpatients with a clinical diagnosis of vasovagal, situational, or orthostatic syncope (13 patients with clear-cut dehydration or bleeding did not have monitoring); and (5) defini- tive evaluation of any clinical or historical findings suggestive of a cause of syncope. No specific group of patients (e.g., those with Shy-Drager syndrome) were excluded.

Follow-up information regarding recurrences of syncope, presyncopal symptoms, new medical prob- lems, or death was obtained at 3-month intervals for all patients. Information was obtained from the patients themselves, their family, or their physi- cians, and all patients with recurrent symptoms were interviewed with a standardized ques- tionnaire.

Diagnostic Criteria

Orthostatic changes in pulse and blood pressure were measured in a standardized fashion for all pa- tients at the time of our initial evaluation. Blood pressure was measured (by trained research physi- cian assistants) in each arm by a standard cuff sphygmomanometer, and the arm with the higher systolic blood pressure was used for all subsequent measurements. Blood pressure and pulse were re- corded after patients had rested in a supine position for at least 5 minutes. Patients were then asked to stand quietly for 10 minutes, and pulse and blood pressure measurements were repeated immediately upon standing and after 1,2,3,5, and 10 minutes of standing. Zero time was defined as the time at which the first blood pressure was obtained, imme- diately upon standing. If symptoms developed dur-

Diagnostic criteria for the causes of syncope were developed prior to the study and have been de- scribed elsewhere [4]. The assignment of specific etiologies was based on these criteria. Significant orthostatic hypotension was defined as a systolic blood pressure decline of 20 mm Hg or more. Crite- ria for orthostatic hypotension as a cause of syncope required a clinical presentation consistent with or- thostatic hypotension (i.e., syncope in an upright position or upon standing) and excluded patients with another documented cause of syncope (e.g., arrhythmia). Upon testing, patients had to exhibit a symptomatic decline in systolic blood pressure. Or- thostatic hypotension was diagnosed in asymptom- atic patients with a reduction of 20 mm Hg or more in systolic blood pressure only if the minimum standing pressure fell below 90 mm Hg or syncope occurred after evident fluid loss (e.g., bleeding, vomiting).

Statistical Analysis All information from initial evaluation and fol-

low-up was recorded on preceded forms. Associa- tions between differing levels of orthostatic hypo- tension and clinical characteristics were assessed with chi-square analysis or t-tests of independent means. Changes in blood pressure over time were examined using repeated-measures analysis of vari- ance. Recurrence of syncope or presyncope was ana- lyzed using life-table methods, and recurrence rates

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SYNCOPE AND ORTHOSTATIC HYPOTENSION / ATKINS ET AL

TABLE I TABLE II

Selected Characteristics of 223 Patients with Syncope Maximal Change (from supine value) in Standing Systolic Blood Pressure*

Number %

M;;age (range)

Past medical history Diabetes Systolic hypertension* Heart disease’ Medication riskt

Syncope in previous year

upinesystolic blood pressure 160 mm Hgor greater. ongestive heart failure, angina, or prior infarction. ascdilators, diuretics, antihypartensives, or psychotherapeutics.

among different groups were compared using dis- crete survival analysis. The relationship between the degree of orthostatic hypotension and the num- ber of recurrent syncopal episodes on follow-up was analyzed using Poisson regression analysis.

RESULTS Patient Characteristics

During the study period, 307 patients were evalu- ated for loss of consciousness. Forty-three patients refused to participate or were not available and 23 did not meet our criteria for syncope. Of the re- maining 241 patients, 11 were unable to stand for orthostatic measurements of blood pressure (be- cause of physical disability, lack of cooperation, fa- tigue, or refusal) and seven were excluded due to incomplete information. This resulted in a final study group of 223 patients. Standardized evalua- tions were performed at a mean of 1 day after entry into the study. Selected characteristics of this co- hort are shown in Table I.

Orthostatic Blood Pressure The distribution of maximal orthostatic changes

in systolic blood pressure among the 223 subjects is shown in Table II. Sixty-nine subjects (31%) had a decline in systolic blood pressure of 20 mm Hg or more within 10 minutes of standing. This includes eight patients who had a decline of 20 mm Hg or more documented during evaluation in the emer- gency room, but who had lesser degrees of orthosta- sis on our assessment since immediate therapy had been given.

Diastolic blood pressure changes of 10 mm Hg or more were present in only 31 (14%) patients. Changes in mean arterial pressure (calculated as diastolic blood pressure + % [systolic blood pres- sure - diastolic blood pressure]) of 10 mm Hg or more were present in 44 (20%) patients. All but one of these subjects had changes in systolic pressure of an equal or greater magnitude.

Maximal Change (mm Hg)t Number 96

s9 10-19 ii % 20-29 230 2 :2"

alculated from values recorded during lo-minute stand or on initial presentation to emergency room for patients who received immediate therapy. ‘Mean heart rate increase immediately upon standing

TABLE Ill

Differences in Patient Characteristics by Level of Maximum Orthostatic Blood Pressure Change

Orthostasis z20mm Hg

(n = 69)

Orthostasis t20mm Hg (n = 164) p Value

Mean (years) age Mean baseline SBP

(mm Hg) Mean baseline DBP

(mm Hg) Mean number of

medications

SpTzc(OF;dication SymptonYatic (%)

57 48 0.005

134 126 0.007

74 74 0.5

2.2 2.0 0.6

41 38 0.5 34 11 0.001

Syncope in previous year (%) 28 29 0.5

Time to minimum SBP (minutes) 2.2 1.9 0.5

SEP = systolic blood pressure; DBP = diastokc blood pressure.

A comparison of general characteristics of pa- tients with and without marked orthostasis (20 mm Hg or more) is shown in Table III. The presence of orthostatic hypotension was significantly associ- ated with increasing age and higher baseline systol- ic blood pressure, but was not associated with base- line diastolic blood pressure, gender, total number of medications, any specific medications (vasodila- tors, antihypertensives, diuretics, or psychothera- peutics), or prior diagnosis of diabetes or hyperten- sion (data not shown).

Timing of Orthostatic Changes in Blood Pressure The time course of changes in systolic blood pres-

sure on prolonged standing is depicted in Figure 1. Twenty-eight (13%) patients could not stand the entire 10 minutes; 13 of these stood less than 3 minutes before they developed symptoms.

We separated subjects into three groups by their maximal change in systolic blood pressure during the lo-minute stand. In each group, the average change in blood pressure exhibited a similar pattern over time (Figure 1). The change from supine val- ues was greatest immediately upon standing (zero

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SYNCOPE AND ORTHOSTATIC HYPOTENSION / ATKINS ET AL

a +5 - % E O- 'ii, :I" -5 -

EE g g -10 -

til 5 -15 -

6 -20 -

I I I I I I I

supine 0 1 2 3 5 10

Time after standing (minutes)

time), and remained relatively stable over the sub- sequent 10 minutes. By repeated-measures analy- sis, blood pressure did not change significantly from 0 to 10 minutes after standing in any group (F[9,955] = 0.35, p >0.5).

Mean heart rate increases were 10.4 (Group l), 9.6 (Group 2), and 10.7 beats/minute (Group 3) immedi- ately upon standing (p = 0.6). There was a smah decrease in the mean pulse change over the lOminute stand in all three groups (0.5 to 2.8 beats/minute), which was significant (F[5,945] = 4.52, p = 0.001).

The median time to reach minimum standing systolic pressure was 1 minute for all subjects, but shorter (0 minutes) among the 91 patients with a less than 10 mm Hg change. Among 61 patients who met our definition of orthostatic hypotension (20 mm Hg or more), the mean time to reach minimum blood pressure was 2.4 minutes. In eight patients who were treated in the emergency room, the time course before therapy was not available.

In 54 patients, a decline of at least 20 mm Hg occurred within 2 minutes of standing. Only seven

r TABLE IV Prevalence of Orthostatic Hypotension (decline in standing SBP 20 mm Hg or greater) by Cause of Syncope

Diagnosis n/N* (%I

Syncope of unknown etiology Vasovagal Cardiact fM$tatlc hypotensiont

Situationalfl l- SW = systolic 01000 pressure.

2 l/84 (25) 9141 (22)

10/35 (29) 2:;3; ;;;I

6/l 1 (55)

l n = number of patients with orthostatic hypotension; N = total number of patients with various causes cd syncope

t Arrhythmia, conduction abnonality, Infarction, and valvular disease, Orthostatic hypotension, medication, blood loss; nine patients with change less than 20 mm Hg

included on basis of fall in blcod pressure accompanied by symptoms or to SBP less than 90 mm Hg. %aizure, psychogenic, viral syndrome, and heat syncope. fkurring during micturition, defecabon, or cough.

Figure 1. The time course of ortho- static hypotension in patients with a systolic blood pressure (SBP) de- cline of 9 mm Hg or less (Group l), systolic blood pressure decline of 10 to 19 mm Hg (Group 2), and systolic blood pressure decline of 20 mm Hg or greater (Group 3). The data are shown for mean sys- tolic blood pressure reduction for each group at any one time and standard errors. The classification into Group 1, 2, or 3 was on the ba- sis of maximal systolic blood pres- sure reduction during the lo-min- ute stand.

subjects (11%) took longer than 2 minutes to exhibit a decline of this magnitude, and five of these had intermediate changes (10 to 19 mm Hg) by 2 minutes.

Symptoms Forty patients became symptomatic upon stand-

ing for blood pressure measurements, but only 53% of these had a reduction in systolic blood pressure of 20 mm Hg or more. The presence of symptoms was associated with the magnitude of orthostatic hypo- tension for the entire group (p <O.OOl). Patients with and without symptoms did not differ with re- spect to age, baseline systolic pressure, baseline dia- stolic pressure, minimum systolic pressure, or time to reachminimum pressure. However, symptomatic patients were receiving more medications (p <0.02) and had a larger orthostatic increase in pulse (p <O.OOl) than asymptomatic patients.

Among 69 patients with the most severe orthosta- sis (20 mm Hg or more), only 23 (34%) were symp- tomatic; within this group, neither the magnitude nor the timing of the decrease in blood pressure predicted the presence of symptoms (p >0.5).

Prognosis As of January 1990, we had follow-up on 214

(96%) of the 223 patients. For this analysis, only 205 patients with at least 1 year of follow-up were con- sidered. The l-year mortality rate of patients with a systolic blood pressure decline of 20 mm Hg or more was not significantly different from the mortality in the other two groups (p >0.3).

Patients with maximal reductions in systolic blood pressure of at least 20 mm Hg had a cumula- tive recurrent syncope rate of 14%. This rate was not significantly different from the recurrence rate in patients with smaller systolic blood pressure re-

182 August 1991 The American Journal of Medicine Volume 91

ductions. When both syncope and dizziness were considered as endpoints, patients with larger sys- tolic blood pressure decreases (20 mm Hg or more) had a significantly lower recurrence rate than pa- tients with smaller decreases (24% versus 42%, p <0.05). By Poisson regression, patients with larger systolic blood pressure reductions (20 mm Hg or more) had a significantly lower number of recurrent syncopal events on follow-up (p <O.OOl).

Neither presence of orthostatic symptoms nor lower minimum blood pressure (less than 100 mm Hg) identified patients at a higher risk of recurrent syncope. Among the 84 patients with syncope of unknown etiology, 21 had orthostasis of 20 mm Hg or more. Recurrence of syncope in this group (22%) was similar to the recurrence (syncope and dizzi- ness) among patients with mild or no orthostasis (19% and 30%, respectively).

Association of Orthostatic Hypotension with Other Causes of Syncope

Orthostatic hypotension was common among pa- tients for whom other probable causes of syncope were assigned (Table IV). Forty (25%) of the 160 patients with syncope attributed to cardiac disor- ders, vasovagal reaction, or unknown etiology had orthostatic hypotension of 20 mm Hg or greater. Marked orthostatic changes in blood pressure were significantly more common (55%) among patients with situational syncope (occurring after micturi- tion, defecation, or coughing) and significantly less common (5%) among the 21 patients with syncope due to heat, viral illness, or central nervous system problems.

Syncope Attributed to Orthostatic Hypotension Twenty-six patients fulfilled our diagnostic crite-

ria for orthostatic hypotension as a probable cause of syncope. An additional five patients had syncope attributed to medications or blood loss on the basis of prominent orthostasis and clinical setting. Al- though the patients with orthostatic hypotension reached lower standing blood pressure, they were not different with respect to age, medications, base- line blood pressure, or timing of blood pressure changes. Nearly half (48%) of this group were less than 40 years old. Eighteen of 31 patients had iden- tifiable causes of volume depletion (e.g., vomiting, anorexia), and an additional seven were taking car- diac or psychiatric medications that may have pre- disposed to orthostatic hypotension.

COMMENTS Orthostatic hypotension is widely recognized as a

potential cause of syncope [l-6]. However, several issues concerning orthostatic hypotension and its

importance as a cause of syncope are unresolved. Previous studies have not addressed the timing of blood pressure changes during physical examina- tion, the contribution of orthostasis to other causes of syncope, or the association between orthostatic hypotension and recurrent symptoms. We found that systematically measuring blood pressure over 10 minutes detected a large number of patients with an abnormal orthostatic response, most of whom could be identified within 2 minutes of standing. Substantial declines in systolic blood pressure (20 mm Hg or more) were common regardless of the probable cause of syncope.

Specific methods for measuring orthostatic hypo- tension have received limited attention. In three small studies (10 to 39 subjects) of patients with symptomatic orthostatic hypotension, patients with heart disease, or the elderly, the greatest re- duction in blood pressure was reported at 0.5 to 1 minute after standing [23-251. We found similar results among our patients. The median time to reach minimum standing blood pressure was 1 min- ute, and most patients who developed substantial changes in systolic blood pressure (greater than 20 mm Hg decline) did so within 2 minutes of standing.

There are limited data to define a clinically im- portant change in postural blood pressure. A de- cline in systolic blood pressure of 20 mm Hg or greater, which is frequently used to define ortho- static hypotension [8-lo], is common among pa- tients with systolic hypertension [15] and among the elderly; up to 30% of outpatients over age 75 have orthostatic hypotension by this definition [11,16-181. Consequently, some authors have ar- gued that the diagnosis of orthostatic hypotension should be limited to patients with symptomatic changes in blood pressure [10,14]. Our results illus- trate the difficulties in resolving this issue. Large declines in blood pressure and orthostatic symp- toms were not well correlated, and neither identi- fied subjects at higher risk of recurrent symptoms.

We found a high prevalence of orthostatic hypo- tension among patients with syncope. There are at least three potential reasons for this. First, we screened more thoroughly for orthostatic changes than previous studies. Traditional methods of screening for orthostatic hypotension, with a single measure of blood pressure at 1 or 2 minutes, would have detected two thirds of the cases of orthostatic hypotension that we identified with our detailed measurements. However, the prevalence of sub- stantial blood pressure changes among our syncope patients would still be significantly higher (20%) than would be expected in a healthy, age-matched population. We examined data from an earlier se- ries of patients with syncope, whom we screened

SYNCOPE AND ORTHOSTATIC HYPOTENSION / ATKINS ET AL

August 1991 The American Journal of Medicine Volume 91 183

with a single measure of standing blood pressure, and found a comparable proportion (22%) with or- thostatic hypotension (Kapoor WN, unpublished data). Thus, it appears that our methods are not a sufficient explanation of the high prevalence of or- thostatic hypotension.

Second, the prevalence of orthostatic hypoten- sion may reflect the special characteristics of our study population. Orthostatic hypotension can be a common finding in elderly populations [16,17] and was more common (40%) among our syncope pa- tients who were over age 70. However, age alone is unlikely to account for the high prevalence in our study, since the mean age of our patients was 51 years. While data from a comparable population are limited, the Hypertension Detection and Follow- Up Study reported similar levels of orthostasis in only 2% of hypertensive patients aged 30 to 49 and 4% of patients 50 to 69 years old [22]. Furthermore, in our study, orthostatic hypotension was prevalent (23%) even among patients below the age of 60 years.

Third, the presence of orthostatic hypotension may increase the risk of syncope from other causes. We found that a surprising proportion of patients, regardless of cause of syncope, had orthostatic blood pressure changes that would be considered abnormal (i.e., 20 mm Hg or greater). We have pre- viously described the role of orthostatic hypoten- sion in micturition syncope and defecation syncope [26,27], but no previous study has reported the prevalence of orthostatic hypotension in syncope due to cardiac, vasovagal, or unknown causes.

Lipsitz [E] has argued that multiple medical problems may act together in a patient to cause syncope. As a result, an otherwise benign condition, such as orthostatic hypotension, may cause syncope in the setting of other disorders. For example, hypo- tension due to cardiac problems (e.g., arrhythmia or aortic stenosis) may be more profound in associa- tion with underlying orthostatic hypotension. Con- versely, orthostatic hypotension might precipitate arrhythmias in patients with heart disease, by stim- ulating adrenergic pathways or by compromising coronary blood flow. It has been shown that volume depletion can contribute to vasovagal syncope through stimulation of ventricular volume recep- tors [28,29]. Syncope of unknown etiology may also encompass a variety of subtle cardiac or neurologic disorders that could be exacerbated by orthostatic reductions in blood pressure.

We attributed a larger proportion (14%) of cases of syncope directly to orthostatic hypotension than have previous series [l-6]. Although there is no gold standard for assigning cause of syncope, our criteria were comparable with those reported in other se-

ries. This disparity may reflect the more thorough assessment of symptoms and orthostatic changes in blood pressure that we performed during prolonged standing. We were concerned that a lo-minute stand may occasionally precipitate neurally medi- ated syncope as has been described with standing on upright tilt-table testing [30]. We did not find any patients who developed neurally mediated syn- cope, which may be partly because of the brief peri- od of standing during orthostatic blood pressure measurements (i.e., 10 minutes) as opposed to 45 to 60 minutes used for upright tilt-table testing.

We initially hypothesized that patients with larg- er declines in blood pressure (20 mm Hg or greater) would be more likely to have recurrent symptoms. We found that the number of syncopal episodes and the presence of symptoms were lower on follow-up in these patients than in those with a lower (less than or equal to 20 mm Hg) degree of orthostasis. The reasons for this finding are not clear from our study. It is possible that these patients are treated more aggressively or that larger declines are pri- marily due to acute reversible processes. This issue will require further studies.

Orthostatic hypotension was common among pa- tients with syncope of unknown etiology, but equal- ly common in patients with documented causes of syncope. It seems unlikely that orthostatic hypo- tension alone is a cause of unexplained syncope. However, postural changes in blood pressure may contribute to syncope in a subset of these patients.

In conclusion, we found that orthostatic hypoten- sion was common among patients with syncope. Measuring changes during standing for 2 minutes will detect the vast majority of patients with ortho- static hypotension. The prevalence of orthostatic hypotension in patients with syncope was high and orthostatic hypotension was frequently found in patients with syncope from a variety of other prob- lems. The recurrence of symptoms was lower in pa- tients with orthostatic hypotension of 20 mm Hg or greater as compared with those with a lower degree of orthostasis, although the exact reason for this is not clear from the current study.

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