GASTROENTEROLOGY 77:478-483,1979

High Amplitude, Peristaltic Esophageal

Contractions Associated with Chest Pain
and/or Dysphagia
S. B. BENJAMIN, D. C. GERHARDT, and D. 0. CASTELL
The Gastroenterology Division, Internal Medicine Service, National Naval Medical Center and the
Uniformed Services University of the Health Sciences, Bethesda, Maryland

Esophageal manometric tracings obtained using terized by repetitive, nonperistaltic, simultaneous

low-compliance pneumohydraulic infusion systems contractions, is the prototype of motor abnormalities
were reviewed from patients with symptoms of producing this syndrome.‘-4 Prolonged duration and
chest pain and/or dysphagia. Using this system, we increased amplitude of contraction waves are other
report on 7 symptomatic patients with markedly in- motility defects that have been described in DES.”
creased esophageal peristaltic amplitude. Maximal Although previous reports have made reference to a
peristaltic amplitude for these 7 patients (~25-430 variant of spasm associated with abnormalities of
mmHg) was greater than for normals (75-175 amplitude and duration of peristalsis without simul-
inmHg]. Mean peristaltic amplitude for the 7 was 170 taneous contractions,5,” documentation of amplitude
mmHg, which was greater than for normals (81 + 30 measured using low compliance infusion systems
mmHg, mean & 2 SD). This finding is believed to re- having rapid rise rates has not been published. In
flect the sensitivity of currently available manomet- this report, we review our experience with 7 patients
ric systems. It may be possible with these techniques having esophageal contractions of markedly in-
to define more clearly the bulk of presumed esopha- creased amplitude, but peristaltic, and in whom as-
geal dysfunction, which is at present poorly charac- sociated chest pain and/or dysphagia was the pre-
terized. The relationship of clinical symptoms to ab- senting symptom.
normal esophageal motility is often less than
optimal and may result from an inability to define
Methods
“normal” or from inadequacies of currently avail-
able techniques. Our observations of a subset of Subjects
symptomatic patients having peristaltic contractions Manometric tracings were reviewed of 290 patients
with amplitudes exceeding the normal range seem to referred to the Gastroenterology Division, NNMC, for
characterize one form of esophageal motility defect. evaluation of possible esophageal dysfunction during the
This abnormality was seen more frequently than dif- l,%mo period from August 1977 through July 1978, corre-
fuse esophageal spasm in our laboratory. sponding to the introduction in our laboratory of the low
compliance manometric system described below. A diag-
nosis of “nonspecific esophageal motor dysfunction” was
Motor dysfunction of the esophagus has long been made based on the following criteria: (a) symptoms of in-
termittent chest pain and/or dysphagia; (b) abnormal
recognized as a cause of chest pain with or without
esophageal motility other than classic DES, achalasia, or
dysphagia. Diffuse esophageal spasm (DES), charac-
scleroderma. Normal values for laboratory studies with
the same system represent 40 subjects, 20 asymptomatic
Received August 10,1978. Accepted April 16.1979. volunteers, and 20 randomly selected patients with normal
Address requests for reprints to: S. B. Benjamin, M.D., Box 108, studies.
National Naval Medical Center, Bethesda, Md. 20014.
Supported by Department of Navy Clinical Investigation Pro-
gram No. 5-06-530R. Manometric Studies
The opinions or assertions contained herein are the private
views of the authors and are not to be construed as official or as One catheter was constructed using four separate
reflecting the views of the Department of the Navy or the Depart- pieces of polyvinyl tubing. The manometric orifices in the
ment of Defense. four-lumen catheter were 5 cm apart at 90” angles (diame-
0 1979 by the American Gastroenterological Association ter: 4.5 mm: internal diameter of each lumen: 0.8 mm). A
0016-5085/79/090478-06$02.00
September 1979 HIGH AMPLITUDE. PERISTALTIC ESOPHAGEAL CONTRACTIONS 479

pneumohydraulic capillary infusion system (Arndorfer Table 1. Values for Normal Esophageal Peristalsis
Specialties, Inc.) was used for continuous infusion of each
Mean peristaltic pressure in the 81+ 30 mmHg
lumen at a rate of 0.5 ml/min. Each manometric catheter (mean + 2SD)
distal esophagus”
was connected to a transducer (model 267BC, Hewlett- Range of peak pressures” 75-175 mmHg
Packard) and in turn to a direct writing recorder (model Duration of contraction < 7.5 SW
7700, Hewlett-Packard). The compliance of this system is Velocity” 3.2 + 0.2 cm/xc
low, having a pressure rise rate greater than 400 mmHg/
(’Based on data from 20 normal volunteers and 20 randomly se-
sec.’
lected normal manometric studies.
A standard esophageal manometric study was per-
formed with the four-lumen catheter passed nasally or
orally. A station pull-through technique was used to re- mmHg, were significantly greater than for the nor-
cord lower esophageal sphincter (LES) pressures with all mal controls, 75-175 mmHg (P < 0.0001). The mean
four orifices. The LES pressure recorded for each subject peristaltic amplitude was abnormal in 6 of 7 pa-
represented the mean of the four individual pressures, tients. The mean values (ten swallows for each pa-
measured from the mean gastric pressure. The catheter
tient) for these 7 patients, loo-259 mmHg, were sig-
was then positioned with the distal lumen 2 cm above the
nificantly greater than those for normals, 52-110
LES. Ten “wet swallows” (5 cc water bolus) were adminis-
tered, separated at 30 set intervals, to assess peristaltic ac- mmHg (P < 0.0001). Individual peristaltic waves last-
tivity. Amplitude was measured from the.mean of esopha- ing longer than 7.5 set were seen in 5 of 7 patients.
geal baseline to the peak of the peristaltic wave. The Peristaltic contractions were maintained in all pa-
amplitude of persitalsis for each subject represented the tients. No nonconducted wet swallows were ob-
mean value of ten wet swallows. The duration of the indi- served. Velocity of peristalsis was normal, values
vidual peristaltic waves was measured, in seconds, from ranging from 2.8 to 4.3 cm/set. No characteristic ab-
the onset of the major upstroke of the wave to the end of normality of lower esophageal sphincter pressure
the wave. Velocity, in cm/set, was calculated by measur- (LESP) was observed. Two of 7 patients demon-
ing the distance between onset of the rapid upstroke of the
strated LES hypotension; 1 of 7 had increased LESP.
waves at 2 cm and 7 cm above the LES, divided by the
No abnormalities of LES relaxation were identified.
time required for the wave to traverse this 5 cm distance.
Values for velocity represented the mean for all recorded Acid infusion was performed in 6 of 7 patients.
wet swallows. Repetitive contractions were identified as Four patients experienced retrosternal burning dur-
three or more pressure peaks occurring in succession fol- ing acid infusion. Two of these had no associated
lowing a single swallow. manometric alteration. Patient V.F. demonstrated
Acid and saline infusions were performed with the re- broadening of peristaltic waves with increased am-
cording catheter in place in the esophageal body. Normal plitude, and patient G.S. developed simultaneous re-
saline was infused for 5 min, followed by 0.1 NHCl for 10 petitive waves. In addition, patient J.O. developed
min or until the patient became symptomatic. The solu- severe chest pain, at which time the manometric
tions were instilled intraluminally at a rate of 11 cc/min
tracing was consistent with diffuse esophageal
through the most proximal of the four catheter ports using
spasm, showing simultaneous repetitive waves.
a Harvard infusion pump (model 975).
The following case is typical of these patients:

Results
Case Report
Values for the 40 normal subjects are listed in
The patient, V.F., is a 58-yr-old white female with a
Table 1.Mean peristaltic pressure in the distal 10 cm
chief complaint of chest pain and intermittent dysphagia
of the esophagus was 81 + 30 mmHg (mean f 2 SD). to solids and liquids. She had been evaluated for pyrosis
The range of the individual peak pressures was 75- and intermittent dysphagia 5 yr previously. Upper GI se-
175 mmHg. ries at that time was thought to demonstrate hiatal hernia
Of the 290 patients evaluated during the 12-mo with distal stricture. Neither endoscopy nor manometric
study period, there were 10 patients with achalasia, studies were performed, and therapy with periodic dilata-
3 with DES, and 5 with scleroderma. In addition, 20 tion was instituted.
fulfilled the criteria for a diagnosis of nonspecific The patient was initially evaluated at the National
esophageal motor dysfunction. Within this group of Naval Medical Center in December 1976. At that time, she
related a several months’ history of substernal chest pains
20 patients, 7 patients demonstrated a similar syn-
without radiation, unrelated to eating, position, or exer-
drome of high amplitude peristaltic contractions as
cise. The pain was occasionally present for up to 1 wk,
summarized in Table 2. The distinctive motor abnor-
with some relief offered by nitroglycerin but not by anta-
mality of this group of patients was a maximum am- cids. Electrocardiogram was normal. Upper GI series re-
plitude of peristalsis greater than 175 mmHg, the up- vealed tertiary contractions in the distal esophagus and
per limit of normal for our laboratory. The maximal free gastroesophageal reflux. Endoscopy was normal.
peristaltic amplitudes for these 7 subjects, 225-430 Manometry at that time, using the high compliance sy-
Table 2. Clinical Data From Patients With High Amplitude, Peristaltic Esophageal Contractions 6
Patient f3
J.O. T.R. V.F. A.K. G.S. G.O. K.P.
“:
Age 47 81 58 57 67 53 19
Sex F M F F F F F
Symptoms
Chest pain Yes No Yes Yes Yes Yes No
Dysphagia Yes Yes Yes No Yes No Yes
Amplitude of peristaltic
contractions (mmHg)
Maximum 300 300 430 225 280 230 230
Mean 131 160 200 100 197 192 154
Duration of Wave (set)
Maximum 7 7 15 8.5 12 8 8
Mean 5.5 6.1 9.4 5.8 9.3 7.0 4.5
Velocity of peristaltic
contractions (cm/set) 2.9 2.8 3.2 3.3 4.3 3.3 3.4
Simultaneous waves Yes“ No No No Yes” No No
Repetitive waves No No No Yes” No No
Normal peristalsis Yes Yes Yes Yes Yes Yes Yes
LESP (mmHg)
(N = lo-30 mmHg) 4 11 9 10 25 26 34
Nonconducted Swallows 0 0 0 0 0 0 0
Symptoms with manometric
change Yes No No No No No No
Acid infusion
Symptoms Severe chest pain Not performed Burning Burning Burning No Burning
Manometric change Simultaneous Not performed Broadening and No Simultaneous None
repetitive waves and increased amplitude repetitive waves
loss of amplitude
Manometric diagnosis DES/increased Increased amplitude Increased amplitude, Increased amplitude, Increased amplitude, Increased amplitude, Increased amplitude,
amplitude, LES prolonged duration prolonged duration prolonged duration prolonged duration prolonged duration
hypotension
Barium swallow Normal Tortuosity Tortuosity Normal Tertiary contractions Normal Normal

0 With acid infusion.

 September 1979 HIGH AMPLITUDE, PERISTALTIC ESOPHAGEAL CONTRACTIONS 481

ringe pump system, was reported as normal; however, a

review of the tracing retrospectively revealed abnormal-
ities of duration (peristaltic waves 13-15 set in duration)
and amplitude (greater than 200 mmHg), which were not
believed to be abnormal at that time. Using a combination
of nitrates, Valium, and antacids, she was able to control
her pain. In October 1977, she was reevaluated, however,
with a major complaint of intermittent subxyphoid dys-
phagia to both solids and liquids. Her chest pain was
much less. Upper GI series again revealed tertiary con-
tractions (Figure 1) and free gastroesophageal reflux, but
no evidence of stricture. Manometry was repeated using
the low compliance pneumohydraulic capillary infusion
system described in “Methods.” Figure z demonstrates an
example of her peristaltic response to wet swallows. Pro-
longed duration (12-13 set), high amplitude (ZOO-250
mmHg) contractions are apparent. Figure 3 reveals her
manometric response to intraesophageal acid infusion.
Pressures of approximately 400 mmHg are present: dura-
tion up to 15 set is documented. At this time, she com-
plained of substernal burning discomfort but no severe
pain.

Discussion
Although “high amplitude” contractions have
been frequently suggested as a criterion for the diag-
nosis of esophageal spasm, this was often intended
to describe pressures greater than 40-50 mmHg in
the body of the esophagus.’ Precisely what is “ab-
normal” amplitude is unclear and must depend ini-
tially on a redefinition of “normal,” based on data
obtained by currently available low compliance sys-
tems with high pressure rise rates. Utilizing our cur-
rent manometric techniques, we have identified nor-
mal values for mean distal esophageal peristaltic
amplitude to be 81+- 30 (2. SD) mmHg (mean of six to
ten wet swallows in each of 40 normal subjects). In-
dividual peak pressures range from 75 to 175 mmHg.
These values are in keeping with those previously
described using similar methods.“-‘4 We propose
that “high amplitude” contractions should not be Figure 1. Upper gastrointestinal series of patient V.F. (October
1977). demonstrating tertiary contractions in the distal
identified until mean pressures in the body of the
esophagus.
esophagus clearly exceed 120 mmHg (average of ten
peristaltic waves with 30 set between “wet” swal-
lows) or peak pressures are greater than 200 mmHg, disorders, but they did not report actual amplitude
as was demonstrated in our patients. In order to de- levels.“’ The majority of their patients with pre-
termine maximum amplitudes, pressure measure- sumed esophageal-related pain (10/13) had either in-
ments should be obtained in the distal 10-15 cm of creased amplitude (9/13) or increased duration (l/
the esophagus, since previous studies have shown 13). Only 3/13 met their criteria for classic diffuse
that highest amplitudes occur in this region.‘z-‘4 esophageal spasm, which is consistent with our ex-
The present review of our recent experience with perience (3 patients with DES and 7 patients with
symptomatic nonspecific esophageal motor dysfunc- disorders of amplitude). A similar study was re-
tion (NEMD) suggests that abnormalities of ampli- ported by Pope, in which abnormalities of esopha-
tude may be more common than previously recog- geal amplitude were identified in 16 subjects with
nized. This observation is supported by the recent chest pain.‘”
report by Brand et al., in which they drew attention The manometric recordings from our patients
to what may be a large subset of esophageal motor demonstrate primarily disordered amplitude; all
482 BENJAMIN ET AL. GASTROENTEROLOGY Vol. 77. No. 3

duration of 15 set during acid infusion (Figure 3).

Like the patients of Brand et al., 1 of our patients
had pain and not burning induced by acid. This pa-
tient’s motility demonstrated a transition from high
amplitude peristaltic contractions to classic DES (re-
petitive, synchronous contractions) during acid in-
fusion. The observation that acid perfusion may al-
ter motility is not newI and suggests that reflux may
play a role in some patients with symptomatic
esophageal motor disorders. Five patients out of the
6 tested had an abnormal response to acid. Four of
these had burning and 1 developed severe chest
pain. Peristalsis was recorded during this infusion as
described above. One patient (J.D.) developed mano-
metric changes consistent with DES: the other pa-
tient (V.F.) demonstrated increased amplitude and
prolonged duration. It is important to note, however,
that infusion was not required to demonstrate the
abnormalities of amplitude in any of our patients.
Although the symptoms in patient (J.O.) may be acid
Figure 2. Esophageal manometric tracing from patient V.F. Re-
cordings shown are from the distal three catheter lu-
related, there is nothing in our data to suggest that
mens. The bottom tracing is recorded 2 cm above the this disordered amplitude is a secondary phenome-
lower esophageal sphincter, with the middle and top non.
tracings 5 and 10 cm above, respectively. The response It seems unlikely that these patients represent a
to two “wet” swallows is shown, demonstrating peri-
new type of abnormality. Recognition of these forms
staltic contractions with amplitude 250-300 mmHg
above resting esophageal pressure in the most distal
of altered motility is most likely related to recent ad-
position. Prolonged duration (12-13 set) is also present. vances in techniques of esophageal manometry. Syr-
Decreased amplitude is seen in the most proximal inge-pump manometric systems with large bore in-
wave in response to a wet swallow. fusion tubing are associated with high compliance
and an inability to record true amplitude of esopha-
having peak pressures far above the accepted nor- geal peristalsis in the absence of prohibitive flow
mal for our laboratory (Table 1). Both mean and rates causing large intraluminal volumes likely to
peak peristaltic amplitudes were significantly in- produce secondary peristalsis.’ The minimally com-
creased above normals (P < 0.001). One of these pa- pliant hydraulic-capillary infusion systems yield
tients showed peak pressures over 400 mmHg and high fidelity recordings of esophageal pressures and,

250 -!

Figure 3. This figure demonstrates response to acid

infusion in patient V.F. Catheter is posi-
tioned as in Figure 2. Pressures of 400
mmHg above resting esophageal baseline
with a duration of 15 set are present in
the most distal position. Note the de-
creased velocity of peristalsis seen in the
distal esophagus as compared with the
proximal esophagus.
September 1979 HIGH AMPLITUDE, PERISTALTIC ESOPHAGEAL CONTRACTIONS 483

in particular, allow the recording of high amplitude diologic and manometric observations. Ann Intern Med
contractions in the esophageal body.’ 61:914-923,1964
7. Arndorfer R: Improved infusion system for intraluminal
esophageal manometrics. Gastroenterology 73:23-27,1977
8. Kramer P, Fleshler B, McNally E, Harris LD: Oesophageal
Summary sensitivity to Mecholyl in symptomatic diffuse spasm. Gut
8:120-127,1967
In this report, we describe 7 cases of peri- 9. Kramer P, Harris LD, Donaldson RM: Transition from symp-
staltic pressures that reached maximum levels of tomatic diffuse spasm to cardiospasm. Gut 8:115-119,1967
10. Brand D, Martin D, Pope CE: Esophageal manomctrics in pa-
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ticnts with angina-like chest pain. Am J Dig Dis 22:300-304,
associated with secondary symptoms of chest pain
1977
or dysphagia. The pattern of high amplitude peri- 11. Hollis JB, Caste11 DO: Amplitubc of esophageal peristalsis as
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12. Pope CE II: Effect of infusion on force of closure measure-
quency through the use of modern technology.
ments in the human esophagus. Gastroentcrology 58:616-624,
1970
13. Dodds WJ, Hogan WJ, Reid DP, et al: A comparison between
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