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Amplitude of Esophageal Peristalsis as Determined by Rapid Infusion
Vol. 63, No.3
GASTROENTEHOLOGY
Copyright @ 1972 by The Williams & Wilkins Co.
Printed in U.S.A.
AMPLITUDE OF ESOPHAGEAL PERISTALSIS AS DETERMINED BY RAPID INFUSION JOSEPH DoNALD
B. HOLLIS, LIEUTENANT COMMANDER, AND 0. CASTELL, CoMMANDER, MEDICAL CoRPS,
UNITED STATES NAvY
Gastroenterology Branch, Internal Medicine Service, Naval Hospital, Philadelphia, Pennsylvania
A new method has been developed to measure amplitude of esophageal peristalsis. In normal subjects a triple lumen polyvinyl catheter connected to external transducers was used to measure amplitude of esophageal contractions after 5-ml swallows with infusion rates from 1 to 23 ml per min. A hyperbolic pressure response curve is obtained to increasing infusion rate. Linear transformation of this curve using a reciprocal plot allows calculation of the maximal amplitude. This calculated maximal response was obtained for each of the normal subjects at points 5 and 10 em above the lower esophageal sphincter. The calculated maximal response values ranged from 54 to 254 mm Hg, but were quite reproducible (r = 0.95) in the same subject. Esophageal amplitude measured directly using the new Honeywell intraesophageal transducer confirmed the high values obtained with rapid infusion speed. There was high correlation (r = 0.99) in all subjects studied between the calculated maximal response value and peristaltic amplitude measured directly when these two systems were used simultaneously. Previous methods of measuring amplitude of esophageal contractions have been inaccurate. Modification of technique with currently used infusion systems will allow accurate quantitation of peristaltic amplitude. Intraluminal manometry has been widely used for the evaluation of esophageal peristalsis and sphincter function. It has been shown that a slow, constant infusion of fluid into the recording catheter allows for better estimation of sphincter strength than a fluid-filled uninfused system.'· 2 Previous studies of amplitude of esophageal contractions in normal subjects and in various diseases have been performed using either an uninfused or slow infusion system. In a recent report, Pope 3 has Received January 17, 1972. Accepted April 13, 1972. Address reprint request to: Dr. Joseph B. Hollis, Naval Hospital, Philadelphia, Pennsylvania 19145. The opinions expressed herein are those of the authors and cannot be construed as reflecting the views of the Navy Department or of the Na val Service at large.
shown that a higher infusion rate of 2.4 cc per min allowed exact prediction of pressure in an in vitro esophageal model. In this paper, the results of an in vivo study on the effect of increasing infusion rates on measurement of amplitude of esophageal contractions in normal subjects are reported.
Methods Subjects. Studies were performed in 24 healthy male subjects having a mean age of 25 years (range 19 to 38 years) . None of the subjects gave a history of dysphagia or chronic heartburn. All studies were done after a minimum of a 4-hr fast. Esophageal manometry. Amplitude of esophageal contraction was measured using two systems. The first system (infusion study) consisted of three water-filled polyvinyl tubes, 1.4 mm in internal diameter, each connected
417
418
HOLLIS AND CASTELL
Vol. 63, No. 3
to an external transducer by means of a threethus obtained by both methods from the same way stopcock. Each stopcock was connected site, 10 em above the lower esophageal by a short length of polyvinyl tube to a 50-cc sphincter. The same 10 infusion rates (1 to syringe mounted in a constant infusion pump 23 cc per min) as previously described were (Harvard Apparatus Co., Model no. 975). used and compared with the direct transducer The tubes were arranged so that intraluminal measurement. These studies were performed pressures were recorded at three points 5 em in 10 normal subjects. apart through lateral orifices 1.2 mm in diamSeal-time study. The polyvinyl tube used to eter. The second system (direct transducer) measure intraluminal pressures was placed of measuring amplitude of esophageal contrac- in an empty pan and one of the orifices intertion consisted of a f1exible tube containing three mittently sealed with a finger for 2-sec intersmall (5 mm diameter) pressure transducers vals as measured with a stopwatch. Two repetispaced 5 em apart (Honeywell Inc. , Model 31 tive sealing pressures, separated by 30-sec inProbe). This system allows measurement of tervals, were recorded at increasing infusion esophageal pressures directly by the intra- rates and the mean amplitude for each rate was luminal placement of the transducers conused for calculations. This method was retained in the tube assembly. peated using 4-sec sealing periods. Pressures using both systems were graphed Results on a multichannel direct-writing recorder. Studies were done with the subject in a supine Infusion study. Figure 1 is a schematic position. Belt pneumographs were placed representation of esophageal contraction. around the chest and over the larynx to record On the left is a typical peristaltic wave respirations and swallowing, respectively. seen at a slow infusion rate. In the center Infusion study. This study was performed is shown the wave form seen with a rapid in 14 subjects. The fluid-filled tube assembly infusion rate. These two wave forms are was positioned so that intraluminal pressures superimposed on the right. The flat, were recorded simultaneously from the lower esophageal sphincter (distal orifice) and 5 em broad wave seen with slow infusion rep(middle orifice) and 10 em (proximal orifice) resents a pump artifact. This may be above the sphincter. Esophageal peristaltic explained by"the fact that at the onset of pressures were recorded throughout a range contraction, esophageal squeeze seals off of 10 infusion rates from 1 cc to 23 cc per min. the recording orifice of the catheter. PresA 5-cc water bolus was used to initiate perisure buildup in the system is dependent stalsis. Two swallows, separated by a 30-sec on the rate of infusion. Since peristalsis is interval, were recorded at each infusion rate a dynamic event, the orifice is sealed for a nd the mean amplitude for each rate used only a short time. With slower infusion, for calculation. Amplitude of contraction was measured as the change in pressure from the the seal opens on the down curve of the peak of the resting esophageal pressure (endrelaxation phase of the contraction wave expiratory phase) to the peak of the contracwhen the pressure in the catheter exceeds tion wave. This was done to correct the base external pressure. Thus, the broad, flatline pressure shift caused by rapid infusion . tened waves seen at slow infusion rates Direct transducer study . This study was are a pump artifact, with the upstroke performed in 7 of the above 14 subjects. The dependent on the rate of infusion. By inassembly was positioned with the distal recording site in the lower esophageal sphincter as described above. Esophageal amplitude (\ I I was calculated for 20 swallows, which were I I I I separated by 30-sec intervals. Simultaneous study. A tube assembly was ~ constructed to allow use of both systems of SLOW RAPID PUMP INFUSION INFUSION ARTIFACT measurement simultaneously. A polyvinyl tube (1.4 mm inner diameter) with one orifice FIG. 1. Schematic representation of esophageal was attached by silk sutures to the direct contraction wave forms recorded with slow infusion transducer assembly so that the orifice was (left), rapid infusion (center), and both forms super· located at the same level as the proximal diimposed (right) illustrate pump artifact. Explanarect transducer. Esophageal pressures were tion in text.
September 1972
419
AMPLITUDE OF ESOPHAGEAL PERISTALSIS
creasing the infusion rate, higher pressures will be recorded. Theoretically, at a sufficiently rapid infusion rate, the pressure in the catheter will have time to rise to the true value of the seal. Higher infusion rates should then fail to give higher pressures. This hypothesis is supported by figure 2. Peristaltic amplitude after 5-cc swallows recorded from the proximal and middle orifices in 1 subject is plotted against infusion rate. The hyperbolic curves indicate that increased amplitude of esophageal contraction is obtained by increasing infusion rate, until a rate is reached which results in near-maximal pressure. Figure 3 illustrates the result of a linear transformation of these curves obtained by a reciprocal plot of amplitude of esophageal contraction (Y axis) against infusion rate (X axis). The reciprocal of the Y intercept defines the "calculated maximal response." This represents the calculated maximal limit of the system and, therefore, should give the true amplitude of esophageal squeeze. The calculated maximal response for the proximal and middle orifice in the subject shown in figures 2 and 3 was 118 mm Hg and 77 mm Hg, respectively. Table 1 shows the calculated maximal
•
•
X
10
INFUSION SPEED
(mlfmin)
FIG. 2. Relation of recorded peristaltic amplitude to increasing infusion speed at both proximal (dots) and middle (X) recording sites for 1 normal subject.
.00
.20
.40
.60
.80
1.0
Yls FIG. 3. Linear transformation of curves shown in figure 2 obtained by plotting reciprocal of amplitude (1 /A) against recriprocal of infusion speed (1/IS). Calculated maximal response is defined by reciprocal of Y intercept. 1. Calculated maximal response of peristaltic amplitude for normal subjects
TABLE
Subject
1 2 3 4 5 6 7 8 9 10 11 12 13 14
Proximal
Middle
(mm Hg)
(mm Hg)
54 62 71 71 77
80 87 100 103 118 132 133 138 254
82 70 72 98 92 86 101 69 54 77 108 125 150 155
response for all 14 normal subjects. The values indicate much higher peristaltic amplitudes than previously described using uninfused or low infusion systems. Furthermore, the table shows a wide range of calculated maximal response for these normal subjects. However, despite the marked variations between individuals,
420
Vol. 63, No. 3
HOLLIS AND CASTELL
the calculated maximal response is reproducible in the same subject as shown in figure 4. High correlation (r = 0.98) was obtained between the calculated maximal response on two separate occasions for 5 subjects. Direct transducer study. The mean amplitude of contraction for 20 repetitive swallows using the direct transducer on a subsequent day of testing was compared with the calculated maximal response in 7 of these subjects (fig. 5). There was high correlation (r = 0.95) between the mean peristaltic amplitude (direct transducer) and the calculated maximal response. Simultaneous study. Figure 6 shows the results obtained in 10 normal subjects using the two measuring systems simultaneously at the same site 10 em above the sphincter. Again there was high correlation (r = 0.99) between the two systems. The calculated maximal response using only four infusion rates of 1.61 cc per min, 3.15 cc per min, 6.17 cc per min, and 12.1 cc per min was compared with the calculated maximal responses using 10 infusion rates as previously described. There was high correlation (r = 0.99) between the calculated maximal responses derived using these two methods (table 2). High correlation (r = 0.99) was also found
160
AMPLITUDE [mmHg]
120
CMR 80
r=0.9S
40 ·
o~-----.~o----~.o------1~20----~160
DIRECT
TRANSDUCER
5. Comparison of calculated maximal response (CMR) and mean amplitude obtained with the direct transducer at both proximal and middle recording sites on subsequent days. FIG.
250
AMPLITUDE /
[mmHII]
./ /
/
200
/ /
/
CMR
150
100
•" ~
/
,:,•
/
/ /
r •0.9t
7
50
/
...
/
/ /
/ / / /
AMPLITUDE
50
[mmHg] 160
100
DIRECT
150
200
2.50
TRANSDUCER
FIG. 6. Comparison of calculated maximal response (CMR) and mean direct transducer amplitude recorded simultaneously for 10 subjects.
1~0
DAY 2 10
40
40
10
I 20
160
DAY 1
FIG. 4. Calculated maximal response on 2 separate days from the proximal and middle recording sites for 5 normal subjects.
between the calculated maximal response from four infusion rates and the mean peristaltic amplitude using the direct transducer (table 2) . Seal-time study. As expected, the pressures recorded with increasing infusion rates during mechanical sealing of the recording orifice for 2-sec and 4-sec intervals showed a linear relationship (fig. 7). The results further substantiate the concept that pressure buildup, when
September 1972
AMPLITUDE OF ESOPHAGEAL PERISTALSIS
2. Comparison of peristaltic amplitude m easured as calculated maximal response and with direct transdu cer
TABLE
Subject
1 2 3 4 5 6 7 8 9 10
CMR-10"
CMR-4"
DT•
(mm Hg )
(mm Hg)
(m m Hg)
62 68 80 101 112 120 137 140 146 227
61 69 80 113 117 128 153 146 137 224
68 58 74 108 108 123 143 139 148 219
"---y---.J "---y---.J r = 0 .99 r = 0 .99 a Calculated maximal response (CMR) at 10 infusion rates. " Calculated maximal response (CMR) at four infusion rates. c Direct transducer (DT) (mean of 20 swallows) .
... 4SEC 2SEC
r = 0.991
r - 0 .996
PRESSURE
•
lmmHg)
10
12
FIG. 7. Relation of pressure t o infusion rate with mechanical sealing of recording orifice for 2 and 4 sec.
the recording orifice is sealed, is dependent on the rate of infusion. Discussion Amplitude of esophageal contractions (squeeze) has been studied in normal subjects4·6 after various drugs 6· 7 and in various disease processes. 8 - 1 3 These studies were performed using either uninfused or slowly infused catheters (3 to 4 cc per hr). Our study, and that of Pope, 3 indicate
421
that these previous methods have underestimated true esophageal squeeze. The results of our in vivo study on the effect of increasing infusion rates on measurements of amplitude of esophageal contractions in normal subjects show a hyperbolic pressure response curve. The calculated maximal response, defined by the Y intercept of the linear transformation of the curve, represents the theoretical true amplitude of esophageal squeeze. Our results show that true amplitude of esophageal contractions is much higher than values previously reported using an uninfused or low infusion system. Furthermore, amplitude is higher than that obtained by Pope with an infusion rate of 2.4 cc per min. However, the external pressure applied to that in vitro model was less than 40 mm Hg, which was readily measured by an infusion rate of 2.4 cc per min. Application of higher external pressures, as 100 mm Hg, to such a system would presumably not have been so readily measured at this infusion rate. Despite the marked variations of calculated maximal response among normal individuals, the values are reproducible in the same subject. Furthermore, four infusion rates are sufficient to calculate a reliable maximal response, since these values are similar to those from 10 infusion rates (r = 0.99). Quite recently, a transducer assembly has become available which has the capacity to measure pressures directly by placement of three small transducers in the esophageal lumen. In all subjects studied, there was high correlation between the mean peristaltic amplitude from the direct transducer and the calculated maximal response amplitude from the linear transformation of the hyperbolic pressure response curve to increasing infusion rate. The practicality of using the newly available intraesophageal direct transducer, which is a very delicate, heat-sensitive, and expensive instrument has yet to be determined. Meanwhile, one can continue using the inexpensive polyvinyl
422
HOLLIS AND CASTELL
tubes connected to durable, time-tested, external transducers in evaluating esophageal peristalsis. True amplitude of esophageal squeeze can be determined by using the four infusion speeds as described and by deriving the calculated maximal response. This method should have potential for study of esophageal peristalsis in disease and of the effect of pharmacological agents.
8.
REFERENCES
9.
1. Winans CS, Harris LD : Quantitation of lower · esophageal sphincter competence. Gastroenterology 52:773- 778, 1967 2. Pope CE: A dynamic test of sphincter strength: Its application to the lower esophageal sphincter. Gastroenterology 52:779-786, 1967 3. Pope CE: Effect of infusion on force of closure measurements in the human esophagus. Gastroenterology 58:616-624, 1970 4. Texter EC, Smith HW, Moeller HC, et a!: Intraluminal pressures from the upper gastrointestinal tract. Gastroenterology 32: 1013-1024, 1957 5. Pert JH, Davidson M, Almy TP, et al: Esophageal catheterization studies. 1. The mechanism
6.
7.
10.
11.
12. 13.
Vol. 63, No . 3
of swallowing in normal subjects with particular reference to the vestibule (esophago-gastric sphincter) . J Clin Invest 38:397-406, 1959 Nagler RE, Spiro HM: Serial esophageal motility studies in asymptomatic young subjects. Gastroenterology 41:371-379, 1961 Kantrowitz PA, Siegel CI, Hendrix TR: Differences in motility of the upper and lower esophagus in man and its alteration by atropine. Bull Johns Hopkins Hosp 118:476-491, 1966 Creamer B, Donohue FE, Code DF: Pattern of esophageal motility in diffuse spasm. Gastroenterology 34:782-796, 1958 Mandelstram P , Siegel CI, Lieber A, et al: The swallowing disorder in patients with diabetic neuropathy-gastroenteropathy. Gastroenterology 56:1- 12, 1969 Fischer RA, Ellison GW, Thayer WR, et al: Esophageal motility in neuromuscular disorders. Ann Intern Med 63 :229- 248, 1965 Siegel CI, Hendrix TR, Harvey JC: The swallowing disorder in myotonia dystrophica. Gastroenterology 50:541-550, 1966 Christensen J: Esophageal manometry in myxedema. Gastroenterology 52: 1130- 1138, 1967 Creamer B, Andersen HA, Code CF: Esophageal motility in patients with scleroderma and related diseases. Gastroenterology 86:763-775, 1956
GASTROENTEHOLOGY
Copyright @ 1972 by The Williams & Wilkins Co.
Printed in U.S.A.
AMPLITUDE OF ESOPHAGEAL PERISTALSIS AS DETERMINED BY RAPID INFUSION JOSEPH DoNALD
B. HOLLIS, LIEUTENANT COMMANDER, AND 0. CASTELL, CoMMANDER, MEDICAL CoRPS,
UNITED STATES NAvY
Gastroenterology Branch, Internal Medicine Service, Naval Hospital, Philadelphia, Pennsylvania
A new method has been developed to measure amplitude of esophageal peristalsis. In normal subjects a triple lumen polyvinyl catheter connected to external transducers was used to measure amplitude of esophageal contractions after 5-ml swallows with infusion rates from 1 to 23 ml per min. A hyperbolic pressure response curve is obtained to increasing infusion rate. Linear transformation of this curve using a reciprocal plot allows calculation of the maximal amplitude. This calculated maximal response was obtained for each of the normal subjects at points 5 and 10 em above the lower esophageal sphincter. The calculated maximal response values ranged from 54 to 254 mm Hg, but were quite reproducible (r = 0.95) in the same subject. Esophageal amplitude measured directly using the new Honeywell intraesophageal transducer confirmed the high values obtained with rapid infusion speed. There was high correlation (r = 0.99) in all subjects studied between the calculated maximal response value and peristaltic amplitude measured directly when these two systems were used simultaneously. Previous methods of measuring amplitude of esophageal contractions have been inaccurate. Modification of technique with currently used infusion systems will allow accurate quantitation of peristaltic amplitude. Intraluminal manometry has been widely used for the evaluation of esophageal peristalsis and sphincter function. It has been shown that a slow, constant infusion of fluid into the recording catheter allows for better estimation of sphincter strength than a fluid-filled uninfused system.'· 2 Previous studies of amplitude of esophageal contractions in normal subjects and in various diseases have been performed using either an uninfused or slow infusion system. In a recent report, Pope 3 has Received January 17, 1972. Accepted April 13, 1972. Address reprint request to: Dr. Joseph B. Hollis, Naval Hospital, Philadelphia, Pennsylvania 19145. The opinions expressed herein are those of the authors and cannot be construed as reflecting the views of the Navy Department or of the Na val Service at large.
shown that a higher infusion rate of 2.4 cc per min allowed exact prediction of pressure in an in vitro esophageal model. In this paper, the results of an in vivo study on the effect of increasing infusion rates on measurement of amplitude of esophageal contractions in normal subjects are reported.
Methods Subjects. Studies were performed in 24 healthy male subjects having a mean age of 25 years (range 19 to 38 years) . None of the subjects gave a history of dysphagia or chronic heartburn. All studies were done after a minimum of a 4-hr fast. Esophageal manometry. Amplitude of esophageal contraction was measured using two systems. The first system (infusion study) consisted of three water-filled polyvinyl tubes, 1.4 mm in internal diameter, each connected
417
418
HOLLIS AND CASTELL
Vol. 63, No. 3
to an external transducer by means of a threethus obtained by both methods from the same way stopcock. Each stopcock was connected site, 10 em above the lower esophageal by a short length of polyvinyl tube to a 50-cc sphincter. The same 10 infusion rates (1 to syringe mounted in a constant infusion pump 23 cc per min) as previously described were (Harvard Apparatus Co., Model no. 975). used and compared with the direct transducer The tubes were arranged so that intraluminal measurement. These studies were performed pressures were recorded at three points 5 em in 10 normal subjects. apart through lateral orifices 1.2 mm in diamSeal-time study. The polyvinyl tube used to eter. The second system (direct transducer) measure intraluminal pressures was placed of measuring amplitude of esophageal contrac- in an empty pan and one of the orifices intertion consisted of a f1exible tube containing three mittently sealed with a finger for 2-sec intersmall (5 mm diameter) pressure transducers vals as measured with a stopwatch. Two repetispaced 5 em apart (Honeywell Inc. , Model 31 tive sealing pressures, separated by 30-sec inProbe). This system allows measurement of tervals, were recorded at increasing infusion esophageal pressures directly by the intra- rates and the mean amplitude for each rate was luminal placement of the transducers conused for calculations. This method was retained in the tube assembly. peated using 4-sec sealing periods. Pressures using both systems were graphed Results on a multichannel direct-writing recorder. Studies were done with the subject in a supine Infusion study. Figure 1 is a schematic position. Belt pneumographs were placed representation of esophageal contraction. around the chest and over the larynx to record On the left is a typical peristaltic wave respirations and swallowing, respectively. seen at a slow infusion rate. In the center Infusion study. This study was performed is shown the wave form seen with a rapid in 14 subjects. The fluid-filled tube assembly infusion rate. These two wave forms are was positioned so that intraluminal pressures superimposed on the right. The flat, were recorded simultaneously from the lower esophageal sphincter (distal orifice) and 5 em broad wave seen with slow infusion rep(middle orifice) and 10 em (proximal orifice) resents a pump artifact. This may be above the sphincter. Esophageal peristaltic explained by"the fact that at the onset of pressures were recorded throughout a range contraction, esophageal squeeze seals off of 10 infusion rates from 1 cc to 23 cc per min. the recording orifice of the catheter. PresA 5-cc water bolus was used to initiate perisure buildup in the system is dependent stalsis. Two swallows, separated by a 30-sec on the rate of infusion. Since peristalsis is interval, were recorded at each infusion rate a dynamic event, the orifice is sealed for a nd the mean amplitude for each rate used only a short time. With slower infusion, for calculation. Amplitude of contraction was measured as the change in pressure from the the seal opens on the down curve of the peak of the resting esophageal pressure (endrelaxation phase of the contraction wave expiratory phase) to the peak of the contracwhen the pressure in the catheter exceeds tion wave. This was done to correct the base external pressure. Thus, the broad, flatline pressure shift caused by rapid infusion . tened waves seen at slow infusion rates Direct transducer study . This study was are a pump artifact, with the upstroke performed in 7 of the above 14 subjects. The dependent on the rate of infusion. By inassembly was positioned with the distal recording site in the lower esophageal sphincter as described above. Esophageal amplitude (\ I I was calculated for 20 swallows, which were I I I I separated by 30-sec intervals. Simultaneous study. A tube assembly was ~ constructed to allow use of both systems of SLOW RAPID PUMP INFUSION INFUSION ARTIFACT measurement simultaneously. A polyvinyl tube (1.4 mm inner diameter) with one orifice FIG. 1. Schematic representation of esophageal was attached by silk sutures to the direct contraction wave forms recorded with slow infusion transducer assembly so that the orifice was (left), rapid infusion (center), and both forms super· located at the same level as the proximal diimposed (right) illustrate pump artifact. Explanarect transducer. Esophageal pressures were tion in text.
September 1972
419
AMPLITUDE OF ESOPHAGEAL PERISTALSIS
creasing the infusion rate, higher pressures will be recorded. Theoretically, at a sufficiently rapid infusion rate, the pressure in the catheter will have time to rise to the true value of the seal. Higher infusion rates should then fail to give higher pressures. This hypothesis is supported by figure 2. Peristaltic amplitude after 5-cc swallows recorded from the proximal and middle orifices in 1 subject is plotted against infusion rate. The hyperbolic curves indicate that increased amplitude of esophageal contraction is obtained by increasing infusion rate, until a rate is reached which results in near-maximal pressure. Figure 3 illustrates the result of a linear transformation of these curves obtained by a reciprocal plot of amplitude of esophageal contraction (Y axis) against infusion rate (X axis). The reciprocal of the Y intercept defines the "calculated maximal response." This represents the calculated maximal limit of the system and, therefore, should give the true amplitude of esophageal squeeze. The calculated maximal response for the proximal and middle orifice in the subject shown in figures 2 and 3 was 118 mm Hg and 77 mm Hg, respectively. Table 1 shows the calculated maximal
•
•
X
10
INFUSION SPEED
(mlfmin)
FIG. 2. Relation of recorded peristaltic amplitude to increasing infusion speed at both proximal (dots) and middle (X) recording sites for 1 normal subject.
.00
.20
.40
.60
.80
1.0
Yls FIG. 3. Linear transformation of curves shown in figure 2 obtained by plotting reciprocal of amplitude (1 /A) against recriprocal of infusion speed (1/IS). Calculated maximal response is defined by reciprocal of Y intercept. 1. Calculated maximal response of peristaltic amplitude for normal subjects
TABLE
Subject
1 2 3 4 5 6 7 8 9 10 11 12 13 14
Proximal
Middle
(mm Hg)
(mm Hg)
54 62 71 71 77
80 87 100 103 118 132 133 138 254
82 70 72 98 92 86 101 69 54 77 108 125 150 155
response for all 14 normal subjects. The values indicate much higher peristaltic amplitudes than previously described using uninfused or low infusion systems. Furthermore, the table shows a wide range of calculated maximal response for these normal subjects. However, despite the marked variations between individuals,
420
Vol. 63, No. 3
HOLLIS AND CASTELL
the calculated maximal response is reproducible in the same subject as shown in figure 4. High correlation (r = 0.98) was obtained between the calculated maximal response on two separate occasions for 5 subjects. Direct transducer study. The mean amplitude of contraction for 20 repetitive swallows using the direct transducer on a subsequent day of testing was compared with the calculated maximal response in 7 of these subjects (fig. 5). There was high correlation (r = 0.95) between the mean peristaltic amplitude (direct transducer) and the calculated maximal response. Simultaneous study. Figure 6 shows the results obtained in 10 normal subjects using the two measuring systems simultaneously at the same site 10 em above the sphincter. Again there was high correlation (r = 0.99) between the two systems. The calculated maximal response using only four infusion rates of 1.61 cc per min, 3.15 cc per min, 6.17 cc per min, and 12.1 cc per min was compared with the calculated maximal responses using 10 infusion rates as previously described. There was high correlation (r = 0.99) between the calculated maximal responses derived using these two methods (table 2). High correlation (r = 0.99) was also found
160
AMPLITUDE [mmHg]
120
CMR 80
r=0.9S
40 ·
o~-----.~o----~.o------1~20----~160
DIRECT
TRANSDUCER
5. Comparison of calculated maximal response (CMR) and mean amplitude obtained with the direct transducer at both proximal and middle recording sites on subsequent days. FIG.
250
AMPLITUDE /
[mmHII]
./ /
/
200
/ /
/
CMR
150
100
•" ~
/
,:,•
/
/ /
r •0.9t
7
50
/
...
/
/ /
/ / / /
AMPLITUDE
50
[mmHg] 160
100
DIRECT
150
200
2.50
TRANSDUCER
FIG. 6. Comparison of calculated maximal response (CMR) and mean direct transducer amplitude recorded simultaneously for 10 subjects.
1~0
DAY 2 10
40
40
10
I 20
160
DAY 1
FIG. 4. Calculated maximal response on 2 separate days from the proximal and middle recording sites for 5 normal subjects.
between the calculated maximal response from four infusion rates and the mean peristaltic amplitude using the direct transducer (table 2) . Seal-time study. As expected, the pressures recorded with increasing infusion rates during mechanical sealing of the recording orifice for 2-sec and 4-sec intervals showed a linear relationship (fig. 7). The results further substantiate the concept that pressure buildup, when
September 1972
AMPLITUDE OF ESOPHAGEAL PERISTALSIS
2. Comparison of peristaltic amplitude m easured as calculated maximal response and with direct transdu cer
TABLE
Subject
1 2 3 4 5 6 7 8 9 10
CMR-10"
CMR-4"
DT•
(mm Hg )
(mm Hg)
(m m Hg)
62 68 80 101 112 120 137 140 146 227
61 69 80 113 117 128 153 146 137 224
68 58 74 108 108 123 143 139 148 219
"---y---.J "---y---.J r = 0 .99 r = 0 .99 a Calculated maximal response (CMR) at 10 infusion rates. " Calculated maximal response (CMR) at four infusion rates. c Direct transducer (DT) (mean of 20 swallows) .
... 4SEC 2SEC
r = 0.991
r - 0 .996
PRESSURE
•
lmmHg)
10
12
FIG. 7. Relation of pressure t o infusion rate with mechanical sealing of recording orifice for 2 and 4 sec.
the recording orifice is sealed, is dependent on the rate of infusion. Discussion Amplitude of esophageal contractions (squeeze) has been studied in normal subjects4·6 after various drugs 6· 7 and in various disease processes. 8 - 1 3 These studies were performed using either uninfused or slowly infused catheters (3 to 4 cc per hr). Our study, and that of Pope, 3 indicate
421
that these previous methods have underestimated true esophageal squeeze. The results of our in vivo study on the effect of increasing infusion rates on measurements of amplitude of esophageal contractions in normal subjects show a hyperbolic pressure response curve. The calculated maximal response, defined by the Y intercept of the linear transformation of the curve, represents the theoretical true amplitude of esophageal squeeze. Our results show that true amplitude of esophageal contractions is much higher than values previously reported using an uninfused or low infusion system. Furthermore, amplitude is higher than that obtained by Pope with an infusion rate of 2.4 cc per min. However, the external pressure applied to that in vitro model was less than 40 mm Hg, which was readily measured by an infusion rate of 2.4 cc per min. Application of higher external pressures, as 100 mm Hg, to such a system would presumably not have been so readily measured at this infusion rate. Despite the marked variations of calculated maximal response among normal individuals, the values are reproducible in the same subject. Furthermore, four infusion rates are sufficient to calculate a reliable maximal response, since these values are similar to those from 10 infusion rates (r = 0.99). Quite recently, a transducer assembly has become available which has the capacity to measure pressures directly by placement of three small transducers in the esophageal lumen. In all subjects studied, there was high correlation between the mean peristaltic amplitude from the direct transducer and the calculated maximal response amplitude from the linear transformation of the hyperbolic pressure response curve to increasing infusion rate. The practicality of using the newly available intraesophageal direct transducer, which is a very delicate, heat-sensitive, and expensive instrument has yet to be determined. Meanwhile, one can continue using the inexpensive polyvinyl
422
HOLLIS AND CASTELL
tubes connected to durable, time-tested, external transducers in evaluating esophageal peristalsis. True amplitude of esophageal squeeze can be determined by using the four infusion speeds as described and by deriving the calculated maximal response. This method should have potential for study of esophageal peristalsis in disease and of the effect of pharmacological agents.
8.
REFERENCES
9.
1. Winans CS, Harris LD : Quantitation of lower · esophageal sphincter competence. Gastroenterology 52:773- 778, 1967 2. Pope CE: A dynamic test of sphincter strength: Its application to the lower esophageal sphincter. Gastroenterology 52:779-786, 1967 3. Pope CE: Effect of infusion on force of closure measurements in the human esophagus. Gastroenterology 58:616-624, 1970 4. Texter EC, Smith HW, Moeller HC, et a!: Intraluminal pressures from the upper gastrointestinal tract. Gastroenterology 32: 1013-1024, 1957 5. Pert JH, Davidson M, Almy TP, et al: Esophageal catheterization studies. 1. The mechanism
6.
7.
10.
11.
12. 13.
Vol. 63, No . 3
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