Electrocardiographic changes in gastric freezing

Electrocardiographic changes in gastric freezing

Electrocardiographic changes in gastric freezing Jorge Escudero, M.D.* Manuel Cuan, M.D.” Gustav0 Baz, M.D.** Ignacio Ptrez-Piiiones, M.D.” Mexico...

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Electrocardiographic

changes

in gastric

freezing

Jorge Escudero, M.D.* Manuel Cuan, M.D.” Gustav0 Baz, M.D.** Ignacio Ptrez-Piiiones, M.D.” Mexico City, Mexico

G

astric freezing has been reported since 1958, as a form of treatment forpeptic ulcer or hiatal hernia.1-4 Considerable experience has been gained with this new type of treatment, although at the present time there is no general agreement as to its usefulness. Several electrocardiographic abnormalities have been reported during gastric freezing.5-7 The purpose of this paper is to describe and evaluate the electrocardiographic changes in patients who have undergone such procedures. Material

and

methods

Sixty-four patients with peptic ulcer and/or hiatal hernia that was corroborated by upper gastrointestinal series underwent gastric freezing. In one case the procedure was repeated after 4% months, making a total of 65 studies. Only 1 of the 64 patients had arteriosclerotic heart disease; the rest had no prior symptoms or signs of heart disease. Fifty-six were men and 8 were women. Their ages ranged from 19 to 63 years, with an average of 39.8

vears. Duodenal ulcer was the reason for gastric freezing in 51 patients, hiatal hernia in 5, a combination of both in 7, and marginal ulcer in 2. Freezing was performed with a low-temperature gastric hypothermia machine. Absolute ethyl alcohol was circulated into a stomach-shaped balloon by means of a double-lumen tube. In-going temperatures were -15 to -19 degrees, and out-coming temperatures were -7 to - 10 degrees centigrade. Perfusion time ranged from 55 to 70 minutes. Fifty-four patients had a normal control electrocardiogram. Among the other 10 patients, there was a low voltage in 1, possible left ventricular hypertrophy in 4, questionable right ventricular hypertrophy in 2, incomplete left bundle branch block in 1, incomplete right bundle branch block in 1, and probable electrolytic disturbance with auricular extrasystoles in 1. Diffuse changes in subepicardial ventricular repolarization were present in the patient with arteriosclerotic heart disease. In 55 instances, three traces were taken: one as a control , another during the period of

From the Departments of Cardiology and Gastraenterology, Hospital General de1 Centro Medico National de1 Instituto Mexicano de1 Seguro Social, Mtico, D.F.. M&xico. This paper was presented at the VII Interamerican Congress of Cardiology, Montreal, Canada, June, 1964. Received for publication Feb. 22, 1965. *Department of Cardiology, Hospital General. **Department of Gastroenterology. Hospital General. Address correspondence to: Dr. Jorge Escudero. Instituto Mexicano de1 Seguro Social, Hospital General de1 Centro Medico National. Av. Cuauhtemoc 330. Mexico 7, D.F., Mexico.

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Table I. v-ariations and average values and after gastric freezing Freezing

Ifeart rate

Before

45 to 115 7.5 50 to 145 86 40 to 110 74

During

After

! I

qf heart

rate, AoRS. ‘1zr, and Q-?‘-.I! I,?, brfoue, durinq,

J QKR(degrees) -50 to 130 50 -60 to 130 43 -60 to 120 SO

perfusion, and the third 90 minutes after the procedure had been completed. In 5 cases, six tracings were taken: one prior to freezing, another during it, and the other 4 at 15minute intervals after completion of the procedure. In the last 5 cases, prefreezing and transfreezing electrocardiograms were also taken, and postfreezing electrocardiograms were recorded at the rate of one every 5 minutes until the tracing became normal. Results H~ythm. Normal sinus rhythm was always preserved, except in the patient with coronary insufficiency, in which case coronary sinus rhythm appeared during the perfusion time and remained throughout the postfreezing tracing. Extrasystoles. These were registered in 5 patients (7.7 per cent) during freezing. In 4 of these patients the extrasystoles were supraventricular, one of them having a short run of paroxysmal tachycardia. The other patient presented occasional right ventricular extrasystoles. Supraventricular extrasystoles disappeared in the postfreezing tracing, in contrast to ventricular extrasystoles, which persisted and even increased. The auricular extrasystoles that were registered in the control electrocardiogram of one patient disappeared during gastric freezing. Another patient registered sinus arrhythmia with bradycardia during freezing, which increased at the end of the procedure. Heart rate. The heart rate increased in 48 (73.8 per cent), from 5 to 65 beats per minute, with an average of 24 beats. It decreased in 14 cases (21.6 per cent), from 5 to 50 beats per minute, with an average

~

---.,IT (degrees) 0 to 70 40 -40 to 60 -3 -40 to 70 38

I (1-T-X v (sac-./‘Iou) -5 to 11 1 -2 to 11 4 -5 to 10 1

of 13 beats, and remained without change in 3 cases (4.6 per cent). Ayns developed a shift to the A QRS. left in 39 cases (60 per cent), from 5 to 60 degrees, with an average of 18 degrees. It rotated to the right in 10 cases (15.4 per cent), from 5 to 20 degrees, with an average of 13 degrees, and remained the same in 16 cases (24.6 per cent). AT. AT rotated to the left in 62 cases (95.4 per cent), from 5 to 100 degrees, with an average of 43 degrees. There was no deviation to the right in any case. It remained the same in 3 cases (4.6 per cent). Q-T-&TV.* Q-T-XIV increased in 54 cases (83 per cent), from 0.01 to 0.09 second, with an average of 0.03 second. It decreased in 2 cases (3 per cent), 0.01 second in both, and remained the same in 9 cases (13.8 per cent) (Table I). Wave abnormalities. The T wave decreased its voltage, becoming negative or increasing its previous negativity in Leads Dir, l)irr, and VF, in 95.4 per cent of the cases. The QRS underwent slight changes in voltage in peripheral leads, in connection with the AoRs changes. The P wave, P-R interval, and S-T segment did not show meaningful changes (Figs. 1 and 2). All previous changes described disappeared within the first 5 to 15 minutes after cessation of freezing, except in the patient with arteriosclerotic heart disease, in whom coronary sinus rhythm appeared and posterolateral subepicardial &hernia had a slight increase. No patient complained of angina1 pain during gastric freezing. *Value of the Q-T interval in relationship to the Mean Value, in accordance with Hazett’s formula: Q-T= 0.39 d\/R - R.

ECG changes in gastric freezing

Fig . 1. Electrocardiograms taken the procedure and its normalization

Fig . 2. Case 51: Similar to that the procedure. Case 55: Changes eve r, the pre-existing abnormality

before, during, and after completion

after freezing. of freezing.

Notice

the alteration

of the T wave

seen in Fig. 1 is alteration of the T wave during freezing, with recover in the T wave are not so marked as in the patients with a normal heart of the T wave increased in the tracing after freezing.

31

during

-y after . How-

Discussion

Distention and freezing of the stomach for 1 hour caused the following electrocardiographic changes, listed according to incidence: (a) decrease in voltage, inversion, or increase of pre-existing negativity of T wave in Leads Dir, l.)rII, and VF, with the consequent rotation of A,13to the left; (b) increase in electrical systole (Q-T interval) ; (c) sinus tachycardia; (d) rotation of A&Rs to the left; and (cl temporary extrasystoles. Among these changes, the most important was that demonstrated by the T wave on the diaphragmatic side of the heart. Several hypothesis may be postulated to explain this fact: (1) Alanis and Rlascher,R in experiments with dogs showed that the sustained distention of the gastric walls by an inflated rubber balloon in the stomach resulted in a decrease in coronary output of approximately 10 to 12 per cent, along with an increase in efferent impulses of the sympathetic heart nerves. This occurs through the mechanical stimulation of the gastric tension receptors which send afferent impulses that are conducted b, the vagus and splanchnic nerves. (2) The gastric chemoreceptors are stimulated bq freezing, and coronary vasoconstriction is produced by sympathetic reflex. (3) Horizontalization of the heart occurs because of displacement by the stomach. (4) The subepicardial region of the left ventricle is cooled, which alters its repolarization. The first two hypothesis, which explain T-wave changes by coronary vasoconstriction, decrease in coronary output, and ischemia, would not explain why such alteration is only posteroinferior, instead of being diffuse, as is to be expected. The third hypothesis, horizontal position of the heart displaced b?; the distended stomach, could in fact contribute in some extent to the rotation of AT to the left, with the consequent alterations of the T wave in peripheral leads. However, \ve believe that this explanation is not satisfactory either, since Iye did not find iL shift to the left of i\p and Aalls proportionate to that of AT, as would be expected with a change in the position of the heart. Furthermore, Wilson and Finch9 reported that T-wave changes caused by ingestion of 600 C.C. of cold water were not present

when the sanle amount of hot lemon;~tlc was given. The fourth hypothesis appears to be the most likely explanation of the alteration of the T \\‘aves. The fundus of the distended stomach makes cant art with t hc posterior-inferior region of the left ventricle, as uxs demonstrated radiologicall>~ by Wilson and Finch” in 1923. These authors stated that the cooling of the stoneach is translnitted to the closer superficial areas of the myocardium, lvhich, in turn, delay their repolarization. Since subendocardial areas are not affected in the sanle manner by cooling.“’ recoverqp takes place first in these regions, with the consequent inversion of the repolarization process, which is then from endocardium to epicardium. Thus, with the negativity of the repolarization vectors in front, the epicardial electrodes lvill register negative T waves in those leads facing the diaphragmatic aspect of the heart.” As for the other changes produced in the electrocardiogram by gastric freezing, the increase in electrical systole (Q-T interval) would also be due to the retardation of metabolic processes in the myocardium produced by cooling, \\ith the subsequent delay in ventricular repolarization. Tachycardia ma\’ be explained bar the alreacly mentioned sympathetic reflex stimulation, and probably by the increase in circulating catecholamines due to the stress caused 1~1, the freezing procedure. This same factor could account for the augmented automatism of the heart, bvith the production of extrasystoles. Summary

and

conclusions

A study \vas made of the electrocardiograms of 65 patients with peptic ulcer and/ or hiatal hernia treated by gastric freezing. Freezing was performed by perfusing absolute ethyl alcohol into a gastric balloon for 55 to 70 minutes. Inflow temperatures were - 15 to - lO”C., and outflowtemperatures were - 7 to - 10°C. Electrocardiograms were recorded before, during, and after freezing. The most frequent changes were a decrease in voltage or inversion of the T wave in Leads 1111, r:,III, and VF, prolongation of the electrical systole, and tachycardia. Left deviation of A g 1< were observed s and rxtrasystoles

ECG changes in gastric freezing

with lower incidence. These alterations disappeared slowly within the first minutes after completion of the freezing, except in one patient who previously had arteriosclerotic heart disease. The possible explanations for these changes are discussed.

4.

5.

6.

Addendum

Since completion of this report, gastric freezing has been performed on another patient who had an old myocardial infarction. No electrocardiographic changes were observed during or after freezing.

7.

8. REFERENCES Wangensteen, 0. H., Root, H. D., Jenson, C. B., Itnamoglu, K., and Salmon, P. A.: Depression of gastric secretion and digestion by gastric hypothermia. Its clinical use in massive hematemesis, Surgery 44:265, 1958. Wangensteen, 0. H., et al.: Physiological gastrectomy by gastric freezing. Preliminary report of experimental and clinical study, J.A.M.A. 180:43a, 1962. Peter, E. T., Bernstein, E. F., Sosin, H., Madsem, A. J., Walder, A. I., and Wangensteen, 0. H.: Technique of gastric freezing in the treatment of duodenal ulcer, J.A.M.A. 181:760, 1962.

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10.

11.

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Wangensteen, 0. H., Salmon, P. A., Griffen, W. O., Jr., Paterson, J. R. S., and Farouk, F.: Studies of local gastric cooling as related to peptic ulcer, AnnYSurg. 150:34Z, 1959. Heineken. T. S.. Rich. R. E.. GreifinPer. W.. Stoll, G.’ F., and O’brady, M. J.:“G~&trid freezing. Prelitninary report on ten cases, Am. J. Gastroenterol. 39:648, 1963. Bernstein, E. F., Goodale, R. L., Jr., McFee, A. S., Madsen, A. J., Delaney, J. P., and Wangensteen, 0. II.: Interim report on results of gastric freezing for peptic ulcer. Present indications, limitations and clinical achievement, J.A.M.A. 187:436, 1964. Reynolds, B. M., and Scherl, N. D.: Paroxysmal atria1 fibrillation after gastric freezing, New England J. Med. 270:1301, 1964. Alanis, J., and Mascher, D.: Cambios de la circulacibn coronaria provocados por la actividad refleja, Arch. Inst. Cardiol. Mexico 33:587, 1963. Wilson, F. N., and Finch, R.: The effect of drinking iced-water upon the form of the T deflection of the electrocardiogram, Heart 10:275, 1923. Wilson, F. N., and Hermann, G. R.: An experimental study of incomplete bundle branch block and of the refractory period of the heart of the dog, Heart 8:229, 1921. Cabrera, E.: Teoria y practica de la electrocardiografia, Mexico City, 1963, La Prensa iX’ICdica Mexicana, p. 182.