THE EFFECT OF LOCAL ANESTHETICS ON FETAL HEART RATE* RoY H. PETRIE, M.D. Assistant Professor, Department of Obstetrics and Gynecology Columbia University College of Physicians and Surgeons New York, N.Y.
S INCE local anesthetics have been used for intrapartum paracervical block it has been known that local anesthetics may affect the fetal heart rate. The full impact was not appreciated until continuous monitoring of the fetal heart rate and associated uterine activity was utilized clinically. At present, local anesthetics are used during labor for the following types of obstetric analgesia and anesthesia: paracervical block, pudendal block, subarachnoid block, peridural block, and local cutaneous and vaginal infiltration. Although an effect may not be noted after every procedure, any of these may alter the fetal heart rate. The fetal heart rate as calculated and recorded from a direct fetal electrocardiographic signal normally is between I2o and i6o beats per minute. Changes of short duration associated with uterine contractions are known as periodic patterns. Potentially ominous periodic patterns are of two types: i) late deceleration, occurring just after the onset of the contraction and caused by uteroplacental insufficiency or hypoxia and 2) variable deceleration, occurring in varied shapes and in varied relation to uterine contraction, often falling below go beats per minute, and caused by compression of the umbilical cord. The rate between contractions is called the baseline rate, and alterations in it are known as baseline tachycardia and bradycardia. In addition, there are small fluctuations that result from the fine interaction of the sympathetic and parasympathetic nervous systems upon the fetal heart rate. These are known as beat-to-beat variations or interval differences.1 The mechanisms by which a local anesthetic may alter the fetal heart rate are numerous and not all are known. On some occasions one or more mechanisms may be involved. The simplest cause of a change *Presented as part of a Symposium on Local Anesthetics in Obstetrics held by the Section on Anesthesiology and Resuscitation of the New York Academy of Medicine March 5, 1975.
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in fetal heart rate is direct action of drugs. It is well known that in adults local anesthetics may affect the heart directly. Freeman2 has shown that in the fetus elevated levels of a local anesthetic can cause widening of its QRS complex. Beat-to-beat arrhythmias can be seen during the fetal bradycardia which follows paracervical block. This alteration of the fetal heart rate may represent a direct drug effect. A second influence that can cause an alteration of the fetal heart rate is alteration of uterine activity. Using an on-line quantitative analysis of uterine activity, Miller3 has demonstrated that uterine activity often increases significantly after paracervical block; this, however, is not always followed by fetal bradycardia. The changes in fetal heart rate associated with increased uterine activity are usually of the kind seen in uteroplacental insufficiency. A third mechanism that can bring about changes in fetal heart rate is maternal hypotension with resultant fetal hypoxia, caused by the blockade of the maternal autonomic nervous system. Local anesthetics in high concentrations are known to excite the central nervous system and produce convulsions. By using elevated levels of local anesthetics, Teramo4 has demonstrated convulsions in fetal sheep in utero. With excitation of the fetal nervous system, it would be expected that beatto-beat variability would be increased. With lower concentrations of a local anesthetic, reduction of such differences may be noted; presumably, this is a direct myocardial effect which produces a regulatory result or possibly a depression of the central nervous system. Specific examples of changes in the fetal heart rate resulting from the use of local anesthetics should be considered. The best known is the fetal bradycardia which follows the paracervical block. The exact mechanism is poorly understood. Evidence of direct myocardial effect includes the fact that peak levels of drug are observed in the fetus eight to io minutes after the injection of the local anesthetic;3 this is about the time that most fetal bradycardias of this kind occur.6 This alteration is usually manifested as a change in the baseline fetal heart rate during a period of several minutes, but the bradycardia may persist for hours. The change in fetal heart rate may be preceded and followed by increased vagal tone similar to variable deceleration, but a pattern similar to that of late deceleration can be observed also. There may be more than one cause for the fetal bradycardia which occurs after a paracervical block. This is likely in the light of the data Vol. 52, No. 2, February 1976
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demonstrating that after a paracervical block fetal concentrations of a local anesthetic may exceed concomitant maternal concentrations without resulting in fetal bradycardia and from data demonstrating that increased uterine activity takes place following a paracervical block.5' 11 After the use of local anesthetics in peridural blocks, several investigators7 have observed fetal bradycardia similar to that observed with paracervical block but occurring at a slightly later interval and much less frequently. The alteration in fetal heart rate observed next most often after the use of local anesthetics is the bradycardia which may follow maternal hypotension induced by peridural or subarachnoid block. It should be noted that the supine hypotension syndrome caused by uterine compression of the inferior vena cava can potentiate or be confused with the alteration in fetal heart rate that is induced by peridural or subdural block. This alteration may be of two types: increased vagal tone of the variable deceleration variety and a purer pattern of late deceleration. Mixtures of these two patterns and pure baseline fetal bradycardia can be observed. McDonald8 reported an increase in the incidence of late deceleration with the absence of maternal hypotension in peridural block. He noted that with proper management there was no alteration in the neonatal outcome. The next most common alteration secondary to local anesthetics is dimininution of the beat-to-beat interval differences. This change is observed most often after peridural block but it may be seen also with other procedures in which local anesthetics are used. Blood levels of local anesthetics following pudendal block and cutaneous infiltration are similar to those noted following peridural block.9' 10 Diminution in the beat-to-beat interval differences may represent regulatory effects on fetal heart rate or perhaps a degree of hypoxia. This alteration is now being investigated by dividing the differences into short-term and longterm indices, which are compared with actual drug levels.3 Physicians should be familiar with the effects of local anesthetics on the fetal heart rate. They should understand the changes which may occur in the heart rate and in underlying mechanisms in order to know when therapeutic measures should be undertaken. Otherwise, unwarranted procedures may be performed and fetal damage may result. This knowledge should be second nature to any physician responsible for intrapartum patients who receive local anesthetics. Bull. N. Y. Acad. Med.
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When local anesthetics are used, it is often helpful to have baseline measurements of fetal capillary and maternal free-flowing venous pH and respiratory gases prior to the procedure. If the fetal heart rate is of a configuration not reassuring to the physician, additional study of the fetus is in order. A protocol for general management includes the following steps. The beat-to-beat variability should be observed carefully. If adequate variability is present, the fetus is probably in good condition. If the only alteration in fetal heart rate is loss of beat-to-beat variability, normal variability should return within approximately 30 minutes. If it fails to do so by this time, the pH and repiratory gases in the fetal blood should be determined. If the baseline fetal heart rate falls below ioo beats per minute for longer than IO minutes or if variable or late deceleration persists for more than five to IO minutes, every effort should be made to correct the abnormality. The use of oxytocin should be discontinued, maternal hypotension should be corrected, and oxygen should be given by a tightfitting face mask at five to six liters per minute. The maternal position should be corrected in order to reduce compression of the umbilical cord. If these measures do not correct the fetal heart rate, fetal capillary blood should be collected for determination of pH and respiratory gases. If these determinations also indicate that fetal jeopardy is present, the fetus should be delivered by the method that is safest for fetus and mother. REFERENCES 1. Hon, E. H.: An Atlas of Fetal Heart
Rate Patterns. New Haven, Harty, 1968, pp. 39-243. 2. Freeman, R. K., Gutierrez, N. A., Ray, M. L., Stovall, D., Paul, R. H., and Hon, E. H.: Fetal cardiac response to paracervical block anesthesia, Part I. Amer. J. Obstet. Gynec. 113:583, 1972. 3. Miller, F. C., Petrie, R. H., Quesnel, G., Arce, J. J., Yeh, S. Y., Paul, R. H., and Hon, E. H.: The effect of paracervical block upon uterine activity and fetal heart rate beat-to-beat interval differences. In preparation. 4. Teramo, K., Benowitz, N., Heymann, M. A., KahanpAX, K., Siimes, A., and
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Rudolph, A. M.: Effects of lidocaine on heart rate, blood pressure and electrocorticogram in fetal sheep. Amer. J. Obstet. Gynec. 118:935, 1974. 5. Petrie, R. H., Paul, W. L., Miller, F. C., Arce, J. J., Paul, R. H., Nakamura, R. M., and Hon, E. H.: Placental transfer of lidocaine following paracervical block. Amer. J. Obstet. Gynec. 120:791, 1974. 6. Paul, R. H. and Freeman, R. K.: Fetal cardiac response to paracervical block anasthesia, Part II. Amer. J. Obstet. Gynec. 113:592, 1972. 7. Finster, M. and Schifrin, B. S.: Personal communication.
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8. McDonald, J. S., Bjorkman, L. L., and Reed, E. C.: Epidural analgesia for obstetrics. Amer. J. Obstet. Gynec. 120: 1055, 1974. 9. Paul, W. L., Miller, F. C., Arce, J. J., Paul, R. H., and Hon, E. H.: Unpublished data. tO. Morishima, H. O., Daniel, S., Finster, M., Poppers, P. J., and James, L. S.: Transmission of mepivacaine hydro-
chloride (Carbocaine) across the human placenta. Anesthesiology 27:147, 1966. 11. Gardmark, S.: Studies on acid-base balance, carbohydrate and lipid metabolism in human fetal and maternal blood in clinical and experimental conditions during labour. Dissertation, University of Lund, Sweden, 1974, pp. 87-95.
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