Cerebrospinal fluid pressures during labor

Cerebrospinal fluid pressures during labor

Cerebrospinal fluid pressures during labor ALOIS VASICKA. M.D.* HENRY KRETCHMER, M.D. FRANCIS LAWAS, M.D. Cleveland, Ohio P H Y s 1 o L o G I c A L L...

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Cerebrospinal fluid pressures during labor ALOIS VASICKA. M.D.* HENRY KRETCHMER, M.D. FRANCIS LAWAS, M.D. Cleveland, Ohio

P H Y s 1 o L o G I c A L L Y , the cerebrospinal fluid pressure is regulated by the rate of its production and its absorption. In this respect, the choroid plexus may show individual variations but, generally, the amount and the pressure of spinal fluid depends on the venous pressure in the vascular network of the choroid plexus and the brain tissue. Thus, simply, acute changes in the venous pressures in the brain would reflect the pressures of the spinal fluid. In view of the pronounced hemodynamic changes which are caused by pregnancy and labor, it became of interest to find out what the spinal fluid pressures in the healthy pregnant patient are, what serial changes take place during labor, and what the effect of the uterine contraction alone is on cerebrospinal fluid pressure. Method Simultaneous recording£ of the intraamniotic pressures (Caldeyro-Barcia method) and the lumbar spinal fluid pressures were made in pregnant patients during labor. Four groups of normal healthy patients were

studied: those who were in labor and did not have any medication, those who were medicated and did not have any complaint of pain or urge to bear down, and those who had spinal anesthesia or general anesthesia with or without intubation (with succinylcholine). The serial recording of the intraamniotic pressures has been previously described.4 For the purpose of recording the cerebrospinal fluid pressures, a thin polyethylene catheter was connected with a pressure transducer and direct-writing oscillograph. Since both pressures, that is, intraamniotic and cerebrospinal, were recorded simultaneously on one direct-writing oscillograph, the speed had to be adjusted to the frequency of the uterine contractions in order to obtain an adequate record of the uterine contractility. The small square on the abscissa equals 20 seconds and the large square equals 100 seconds. On the ordinate, the uterine contractions were calibrated so that one square equals 10 mm. Hg and, on the curve of cerebrospinal fluid pressure, one square represents 4 mm. Hg, or 54.5 mm. H 2 0.

From the Department of Surgery, Obstetrics, and Gynecology, and the Department of Anesthesia, Cleveland Metropolitan General Hospital, and Western Reserve University School of Medicine. This investigation was supported in part by Research Grant No. 71161 (Rl) from the National Institutes of Health. United States Public Health Service. *Present address: The University of Texas, Medical Branch, Galveston, Texas.

Spinal fluid pressures in normal pregnant patients in labor fluctuate with breathing between 150 to 270 mm. H 2 0 in patients in the supine position, under basic conditions without sensations of pain or discomfort (Fig. 1). During the painful uterine ccntractions, which reach 60 mm. Hg in intensity and occur every one or one and onehalf minutes, the cerebrospinal fluid pres-

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sures were increased by an additional 108 to 160 mm. H 2 0 or 8 to 16 mm. Hg, at the peak of each contraction. There was no clinical evidence of bearing down, although patients were complaining of pain (Fig. 2). In patients, who were in the right lateral position, the fluctuations of cerebrospinal fluid pressure were practically none with breathing and minimal with uterine contractions (Fig. 3). When 10 mg. of morphine sulfate was given intramuscularly, there was no appreciative rise in cerebrospinal fluid pressure during the uterine contractions. Fluctuations of cerebrospinal fluid pressures not related to uterine contractions, however, were conspicuous (Fig. 4 ). It should be noted that the uterine contractions did not change significantly following this dose of morphine given intramuscularly when the cervix was 6 em. dilated. Only a slight alteration of the intensity and frequency occurred. It became obvious, at this point of the study, that in these patients the spinal fluid pressures and their fluctuations are dependent on the rate of breathing and on bearing down, i.e., on the changes of intrathoracic pressures and on the changes of the intra-abdominal

pressures, both of which can be altered by painful stimuli. In order to elucidate what effect the uterine contraction alone would have on the spinal fluid pressures, the thoracic pressures and intra-abdominal pressures had to be eliminated. The intra-abdominal pressures were eliminated with high spinal anesthesia. Fig. 5 represents a recording of the uterine contractility and the cerebrospinal fluid pressures before and after high spinal anesthesia. In a patient with a fully dilated cervix and the vertex in midplane of the pelvis before the spinal anesthesia, a marked elevation of cerebrospinal fluid pressure is seen to occur with each uterine contraction. There is conspicuous evidence of the bearing down effort of the parturient in that the dome of the contour of each contraction is irregular and hazy. After the spinal anesthesia has been given and a sensory level to T 6 obtained, the contour of the uterine contractions is smooth, indicating that there are no more extrauterine pressures superimposed on the uterus, and the elevations of the spinal fluid pressure, during or between the contractions, disappear. There is another point of interest on this

Fig. 1. Painless uterine contractions. The spinal fluid pressure fluctuates with breathing (between 150 to 270 mm. H ,O ) but not with the amplitude of each contraction.

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INTRA· AMNIOTIC

CEREBRO· SPINAL

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Fig. 2. Pa inful Utf'rinc contrac tions. also with !'ach con traction.

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Huid prt'ss urc fluctuates with breathing and

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Fig. 3. Fluctuations of cerebrospinal fluid were inconspicuous with brea thing and only minimal with uterin e contractions in patients lyin g in right lateral position. Note that medica tion was given.

record. As can be noted from the record, the blood pressure dropped from 120/ 80 to 80/ 60 following the injection .of 3 mg. of tetracaine. Three milligrams of methoxamine was administered intravenously. The blood pressure almost immediately rose to 140/ 90, the uterus responded by a rise of tonus from 20 to 45 rnm. Hg so that an almost tetanic contraction developed. This is a known phenomenon which we have encountered several times and which cannot presently be explained except to say that the effect of methoxamine on the smooth muscle and sudden changes of uterine blood flow have to be considered. It also should be noted that the sudden change of systolic pressure from 80 to 140 did not have conspicuous effect on cerebrospinal fluid pressure.

In order to eliminate both the intraabdominal and the intrathoracic pressures, the intratracheal catheter was introduced so that breathing could continue spontaneously and the Valsalva phenomenon could be eliminated. Fig. 6 shows a record of intraamniotic and cerebrospinal fluid pressures in a patient with an intratracheal tube. The deflections of the cerebrospinal fluid pressure curve which occurred with exaggerated inspiration and expiration are not different from those in a patient without an intratracheal tube. Obviously the patient was unable to bear down, but "bucking" alone shows a marked increase in the cerebrospinal fluid pressure. However, after "bucking" discomfort and pain sensation is eliminated by medication with 75 mg. meperidine hydro-

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chloride and 25 mg. of promethazine, the uterine contractions of 50 mm. Hg in intensity and less than one minute in frequency are not accompanied by elevation of cerebrospinal fluid pressures. The relationship of controlled breathing, cerebrospinal fluid pressure and intra-amniotic pressure is shown in Figs. 7A and 7B. General anesthesia with succinylcholine and intubation was used so that bag breathing under known pressures could be administered by the anesthesiologist. This recording was done on a patient who was to receive a repeat cesarean section and who was in active labor. Respirations during the awakening period were recorded simultaneously with the cerebrospinal fluid pressures. The upper line on Fig. 7 represents the intra-amniotic fluid pressure which did not show any change in this deeply anesthetized patient. With deep muscular relaxation the controlled respirations of 40 'to 50 mm. Hg pressure ~~use only a relatively small 3 to 4 mm. Hg rise in ce~ebrospinal fluid pressure ( 39 to 54 mm. H ~ O ). On the other hand, when the same patient begins to breathe spontaneously with muscular function returning to normal, the cerebrospinal fluid pressures are elevated by 4 to 12 mm. Hg with no more than 20 mm. H g pressure at the expiration. This indicates that the return of the muscular tone in the thorax contributes greatly to the changes in the cerebrospinal fluid pressures. Comment

No claim is made in this study to explain the pathologic physiology of the increased

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cerebrospinal fluid pressure in disease. Only healthy, pregnant patients were studied and an answer was sought to the problem of the effect of uterine contraction alone on the cerebrospinal fluid pressure. During the serial recordings of cerebrospinal fluid pressures and intra-amniotic pressures, sensation of pain, peripheral muscular activity, and changes of intra-abdominal and intrathoracic pressures related to labor have been noted to increase markedly, or perhaps even dangerously, these cerebrospinal fluid pressures. No incontrovertible evidence, however, could be obtained that the uterine contractions alone cause an elevation of cerebrospinal fluid pressure. McCausland and Holmes 3 used serial measurements of cerebrospinal fluid pressure during the contraction and during the relaxation and came to the conclusion that the cerebrospinal fluid pressure during the contraction with the patient not bearing down is slightly to moderately increased. Marx and associates ~ measured the cerebrospinal fluid pressures serially and simultaneously timed uterine contractions, using the usual clinical means of recording the frequency of uterine contractions. Their results indicate that the cerebrospinal fluid pressures are not elevated with contractions. In our study, both pressures, that is intraamniotic, as a result of the uterine contraction, and the cerebrospinal fluid press ure, were recorded simultaneously. The cerebrospinal fluid is not embodied in an elastic environment as is the amniotic fluid ; therefore, the serial changes of the cerebrospinal

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Fig. 4. Effect of morphine sulfate ( 10 mg.) on uterine contractility and cerebrospinal fluid pressures.

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fluid pressure reflect the hydrostatic pressures of the surrounding tissue rather than the active expansion or contraction of the cerebrospinal fluid space. If the change of the cerebrospina l fluid in the normal, healthy pregnant patient under basic conditions, with a regular rate of breathing, regular pulse, and steady blood pressure, reflects the hydrostatic pressure at the venous limb of the cerebral vessels, the uterine contraction does not seem to affect the cerebra l venous pressure. Even though the cerebral venous pressure was not m easured, this assumption could be made on the basis of the serial fluctuation of the cerebrospinal fluid curve during respiration. It is evident that the cerebrospinal fluid pressure readily responds to respirations by pressures of 1 to 3 mm.

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H g which likely reflects directly the range of the cerebral venous pressure changes related to respiration in the patient under basic conditions. Maternal hemodynamic response to uterine contraction has been worked out by Hendricks.' The beginning of a n effective uterine contraction according to Hendricks appears to push a fairly large volume of blood (probably in the range of 250 to 300 c.c. ) rapidly into the central venous reservoir. This results in a rise of central venous pressure of 4 to 6 mm. Hg. Venous femoral pressure is increased as much as 30 mm . Hg. The peripheral venous system in the upper extremity is not affected by the uterine contrac tion . On the basis of our observation of the cerebrospinal fluid pressures in this group of normal pregnant

INTRAAMNIOTIC

CEREBROSPINAL

Fig. 5. Effect of high spinal anesthesia on uterine contractility and th e cerebrospinal fluid pressure. Note the change of uterin e contractility coincident wi th the incrt>asc of blood pressure following th e administration of 3 mg. of methoxamine . With sensory an es thesia (T ") , no eleva tion of spinal fluid pressure during the cont ractions is seen.

INTRAAMNIOTIC

CERUROSPINAL

Fig. 6. Cerebrospinal fluid pressure does not increase during the uterine contraction . ·The Valsalva phenomenon is eliminated by the induction of the intratracheal tube.

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Fig. 7A. Simultaneous recording of intra-amniotic, intratracheal, and cerebrospinal fluid pressure in a patient with general anesthesia and succinylcholine. Uterine contractions arc abolished and the respiration is controlled by bag breathing. Note relatively sma ll elevations of cerebrospinal fluid pressure during the external breathing. 910

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CONTROLLED



RESPIRATION

c Fig. 7B. Continuation of Fig. 7A. Note relatively high elevations of cerebrospinal fluid pressure elevation during the shallow spontaneous breathing. This is contributed to the diminished effect of succinylcholine and return of the thoracic muscular function .

patients in labor, it is safe to assume that the cerebral venous pressure is not altered by uterine contraction alone. It can be summarized, then, that the uterine contraction itself does not increase the cerebrospinal fluid pressure in the healthy pregnant patient. Anxiety, apprehension, and pain associated with uterine contraction, however, cause a rise of cerebrospinal fluid pressure, either directly by the change of heart rate, respiration, and the Valsalva phenomenon, or indirectly by a clinically conspicuous or inconspicuous bearing down. Sudden changes of the intrathoracic pressure and intra-abdominal pressure associated with coughing, vomiting, or vigorous bearing down can cause a rise of cerebrospinal fluid pressure to dangerous levels. From the point of view of practical application of this evidence, there is really no reason why an intradural anesthetic should not be injected

during the contraction in a cooperative and quiet patient who is not bearing down vigorously. Even though the cerebrospinal fluid pressure during the uterine contraction may be increased by 4 to 8 mm. Hg, due to the inconspicuous bearing down or pain sensation, this change of pressure would not be high enough to cause the sudden ascension of the injected anesthetic. It is, therefore, much more important to consider the speed of the injection and the injecting force as factors causing uncontrolled high spinal anesthesia. From an obstetric point of view, this study presents further evidence regarding pressure distribution related to the uterine contraction. Aside from the blood redistribution, which is a relatively small amount and which is taken care of by the heart, the uterine contraction itself does not seem to have an adverse effect on hemodynamics of the

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central nervous system and, therefore, labor should be considered a physiologic process from this point of view. The detrimental factors causing possible harm to the mother or the baby seem to be those which accompany labor, pain, enxiety, bearing down, and apprehension. These should be eliminated either by conditioning or educating the patient and obtaining direct cooperation of the patient or by controlling the patient by medical means such as adequate analgesia and anesthesia.

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Summary

1. The e!Tect of uterine contraction on cerebrospinal fluid pressure has been studied by simultaneous recording of intra-amniotic and cerebrospinal fluid pressures during labor. 2. Changes of intra-abdominal and intrathoracic pressure related to sensation of pain effect the elevation of cerebrospinal fluid during the uterine contraction. :~. Uterine contraction itself does not haYe effect on cerebrospinal fluid pressure.

REFERENCES

L Hendricks, C. H.: AM. J. 0BsT. & GYNEC. 76: 969, i958. 2. Marx, G. F., Zemaitis, M. T,, and Orkin, L. R.: Personal communication.

3. McCausland, A. M., and Holmes, F.: Obst. & Gynec. Year book 11: 148, 1958. 4. Vasicka, A., and Kretchmer, H.: Clin. Obst. & Gynec. 14: 500, 1959.