Craig H. Leicht

Prolongation of lidocaine spinal anesthesia with epinephrine and phenylephrine

: The effect of vasoconstrictors on the duration of lidocaine spinal anesthesia is controversial. We conducted a double-blind study of 28 neurologically normal ASA Class I or II patients to determine the effect of vasoconstrictors (epinephrine and phenylephrine) on the duration of lidocaine spinal anesthesia. The patients were randomized into three groups. All patients received 1.2 mg lidocaine per inch body height, mixed with 0.5 ml of test solution. Group 1 patients received lidocaine plus 0.5 ml normal saline; Group 2 patients received lidocaine plus 0.3 mg epinephrine; Group 3 patients received lidocaine plus 5 mg phenylephrine. Segmental sensory blockade was assessed by pinprick at 2-min intervals for the first 20 min and then every 5 min thereafter. Mean highest level was between T-2 and T-3 for all 3 groups. Time from injection to highest sensory level was similar in Groups 1 and 3, 11.6 +/- 3.57 and 12.0 +/- 5.10 min, respectively, but was significantly prolonged in Group 2, 18.1 +/- 4.33 min. Time for regression by two sensory dermatomes were significantly prolonged in both Groups 2 and 3, 102.9 +/- 18.1 and 105.7 +/- 33.1 min, respectively, compared to 78.1 +/- 12.6 min in Group 1. Times for regression to T-12 was also significantly prolonged in both Groups 2 and 3, 153.7 +/- 27.6 and 156.8 +/- 26.7 min, respectively, compared to 117.71 +/- 10.0 min in Group 1. In the doses used in the present study, both epinephrine and phenylephrine significantly prolong the duration of lidocaine spinal anesthesia.

Continuous spinal analgesia with sufentanil for labor and delivery in a parturient with severe pulmonary stenosis.

I? ulmonary valvular stenosis constitutes roughly lo%-15% of all congenital heart disease (1). The valvular lesion is usually unchanged until late in adult life (2), but in severe cases, secondary infundibular hypertrophy can arise during childhood or early adolescence. This subvalvular lesion can be progressive, resulting in a dynamic right ventricular outflow obstruction. If progression has occurred in the pregnant patient, right ventricular failure can result secondary to an inability to compensate for the increases in heart rate, right ventricular preload, and oxygen consumption associated with pregnancy. This can increase the risk of further maternal morbidity, most commonly manifested as congestive failure, by 50% over patients with nonprogressive stenosis (3). The incidence of spontaneous abortion and fetal death is significantly increased as well (3). Spinal and epidural anesthetic techniques so well suited to the obstetric population are often avoided in this condition because of the potential for cardiovascular side effects. As a result, these mothers frequently receive less than adequate analgesia for their labor and delivery. The use of continuous spinal anesthesia with sufentanil for the management of labor and delivery in a patient with severe combined pulmonic and infundibular stenosis is described in this report.

Prolongation of postoperative epidural sufentanil analgesia with epinephrine.

An early report suggested that the duration of epidural sufentanil postoperative analgesia may also be prolonged by the addition of epinephrine (5). However, data in that study were inconclusive because of the small number of observations made. We speculated that with the addition of a larger dose of epinephrine in a somewhat larger study population, we might be able to demonstrate a statistically significant difference between sufentanil and sufentanil plus epinephrine given epidurally

Fetal heart rate variability and cerebral oxygen consumption in fetal sheep during asphyxia

This study was designed to examine the relationship between fetal heart rate variability and fetal cerebral oxygen uptake. Fetal sheep were chronically prepared with catheters and electrodes to determine cerebral blood flow (microsphere method), cerebral arteriovenous oxygen difference, and the electrocardiogram. An adjustable occluder was placed on the maternal common internal iliac artery to induce fetal asphyxia by reducing uterine blood flow. Fetal heart rate variability tended to decrease in the first 11 min of asphyxia, when cerebral oxygen consumption was approximately 53% of control. Despite stable cerebral oxygen consumption and worsening metabolic acidosis, however, fetal heart rate variability progressively returned towards normal by 36 min. There was no relationship between the depression of FHR variability and the degree of reduction of cerebral oxygen consumption. Nor was there any relationship between an alteration in regional cerebral blood flow or myocardial blood flow and the return of FHR variability with increasing duration of asphyxia. We conclude that there is an association between loss of fetal heart rate variability and reduced cerebral oxygen consumption, but the reduced variability does not persist with time at this degree of reduced cerebral metabolism in fetal sheep. This appears to be at variance with human clinical experience. Among the explanations for this may be insufficiently severe asphyxia, a species difference, removal of an inhibitor to FHR variability, or progressive use of other substrates for metabolism.

PROLONGATION OF LIDOCAINE SPINAL ANESTHESIA WITH EPINEPHRINE AND PHENYLEPHRINE

The effect of vasoconstrictors on the duration of lidocaine spinal anesthesia is controversial. We conducted a double-blind study of 28 neurologically normal ASA Class I or II patients to determine the effect of vasoconstrictors (epinephrine and phenylephrine) on the duration of lidocaine spinal anesthesia. The patients were randomized into three groups. All patients received 1.2 mg lidocaine per inch body height, mixed with 0.5 ml of test solution. Group 1 patients received lidocaine plus 0.5 ml normal saline; Group 2 patients received lidocaine plus 0.3 mg epinephrine; Group 3 patients received lidocaine plus 5 mg phenylephrine. Segmental sensory blockade was assessed by pinprick at 2-min intervals for the first 20 min and then every 5 min thereafter. Mean highest level was between T-2 and T-3 for all 3 groups. Time from injection to highest sensory level was similar in Groups 1 and 3, 11.6 ± 3.57 and 12.0 ± 5.10 min, respectively, but was significantly prolonged in Group 2, 18.1 ± 4.33 min. Time for regression by two sensory dermatomes were significantly prolonged in both Groups 2 and 3, 102.9 ± 18.1 and 105.7 ± 33.1 min, respectively, compared to 78.1 ± 12.6 min in Group 1. Times for regression to T-12 was also significantly prolonged in both Groups 2 and 3, 153.7 ± 27.6 and 156.8 ± 26.7 min, respectively, compared to 117.71 ± 10.0 min in Group 1. In the doses used in the present study, both epinephrine and phenylephrine significantly prolong the duration of lidocaine spinal anesthesia.