Epinephrine Test Dose Research Articles

The Epidural Test Dose in Obstetric Patients

The Epidural Test Dose in Obstetric Patients

Determination of epidural catheter placement using nerve stimulation in obstetric patients

Background and Objectives. Peripheral nerve and spinal cord stimulation techniques have been used for many years. However, electrical stimulation methods rarely have been used to confirm epidural catheter placement. This study examines the practicality of this technique to confirm epidural catheter placement in obstetric patients. Methods. Thirty-nine obstetric patients in labor were studied. An electrocardiography (ECG) adapter (Arrow-Johans) was attached to the proximal end of the epidural catheter (19-gauge Arrow Flextip plus). Then, the lowest milliamperage (1–10 mA) necessary to produce a motor response (truncal or limb movement) was applied using this setup. A positive motor response indicated that the catheter was in the epidural space. This test was performed initially after catheter insertion and repeatedly after incremental local anesthetic doses. Results. The sensitivity and specificity of the new test was 100% and 100%, respectively, with 38 true positive tests and 1 true negative test. The threshold current required to produce a positive test increased after incremental doses of local anesthetic. A case of intravascular epidural catheter migration was detected using this new test. In this case, the patient's increased threshold milliamperage returned to the baseline value within 1 hour, despite having received local anesthetic. Intravascular epidural catheter migration was subsequently confirmed by a positive epinephrine test dose. Thus, this test appears to be a potentially useful method to detect intravascular catheter placement. Conclusion. This study demonstrates that this test may have a role in improving the success rate of epidural anesthesia.

The Efficacy of Epinephrine Test Doses during Combined Spinal-Epidural Anesthesia in Adult Patients

The Efficacy of Epinephrine Test Doses during Combined Spinal-Epidural Anesthesia in Adult Patients

Intrathecal Sufentanil Versus Epidural Lidocaine with Epinephrine and Sufentanil for Early Labor Analgesia

Intrathecal sufentanil provides approximately 2 h of excellent labor analgesia with minimal motor blockade.Epidural sufentanil has received less scrutiny but may provide the same benefits as intrathecal sufentanil. In this study, we compared epidural sufentanil 40 [micro sign]g after a lidocaine with an epinephrine test dose with intrathecal (IT) sufentanil 10 [micro sign]g with respect to onset and duration of analgesia, degree of motor block, side effect profile, and mode of delivery. Seventy ASA physical status I or II parturients in early labor (<or=to4 cm cervical dilation) were randomized to receive either IT sufentanil 10 [micro sign]g with a combined spinal-epidural technique (CSE) or epidural sufentanil 40 [micro sign]g (EP) after epidural catheter placement and testing with 3 mL of 1.5% lidocaine with epinephrine (15 [micro sign]g). After the administration of analgesia, pain scores and side effects were recorded for each patient at 5, 10, 15, 20, and 30 min, and every 30 min thereafter, by an observer blinded to the technique used. The study period was completed when the patients requested additional analgesia. All patients, except one, achieved adequate analgesia with the initial study dose and satisfactorily completed the study. There were no demographic differences between the two groups. Pain relief was rapid for all patients; pain scores were significantly lower at 5 and 10 min in the IT group versus the EP group. The mean duration of analgesia was similar between the EP group (127 +/- 40 min) and the IT group (110 +/- 48 min). No patient experienced any motor block. Side effects were similar between the two groups, except for pruritus-both the incidence and severity were significantly more profound at 5, 10, 15, 20, and 30 min in the IT group. There was no difference in time from analgesic to delivery, incidence of operative or assisted delivery, or cervical dilation at the time of redose. For early laboring patients, epidural sufentanil 40 [micro sign]g after a lidocaine test dose provides analgesia comparable to that of IT sufentanil 10 [micro sign]g with less pruritus. Implications: We compared the efficacy and side effects of intrathecal sufentanil with epidural sufentanil with a local anesthetic test dose for analgesia during labor. Analgesia was equally good, although the intrathecal group experienced more itching. (Anesth Analg 1998;87:331-5)

The Optimal Test Dose of Epinephrine for Epidural Injection with Lidocaine Solution in Awake Patients Premedicated with Oral Clonidine

We attempted to determine the optimal test dose of epinephrine for use with epidural anesthesia in awake patients premedicated with clonidine.Eighty-eight adult patients were randomized into two groups [oral premedication with clonidine 5 [micro sign]g/kg (CLON) or no premedication (CONT)]. Before induction of general anesthesia, heart rate (HR) and blood pressure (BP) were measured for 3 min after the IV injection of 3 mL of 1.5% lidocaine containing epinephrine (0, 1.25, 2.5, 5, 7.5, or 15 [micro sign]g) in a randomized, double-blind manner. We calculated 95% confidence intervals for the peak HR and BP increases induced by each dose of epinephrine. At 7.5 [micro sign]g, epinephrine induced a significantly greater increase in HR and BP in CLON than in CONT. The 95% confidence interval for the HR change induced by 7.5 [micro sign]g of epinephrine in CLON was nearly the same as the accepted standard dose of epinephrine (15 [micro sign]g) in CONT. We conclude that premedication with clonidine enhances HR and BP responses to the IV administration of epinephrine-containing epidural test solutions. Consequently, 7.5 [micro sign]g of epinephrine may be sufficient to enable detection of accidental injection into a blood vessel in awake patients premedicated with clonidine 5 [micro sign]g/kg. Implications: Clonidine, a commonly used preanesthetic medication, alters patients' cardiovascular responses to drugs such as epinephrine. Our randomized, double-blind study suggests that, in awake patients receiving oral clonidine premedication, 7.5 [micro sign]g of epinephrine (half the usual dose) is adequate as an indicator of accidental injection into the epidural vessels during epidural anesthesia. (Anesth Analg 1998;86:1010-4)

2-Chloroprocaine and bupivacaine are unreliable indicators of intravascular injection in the premedicated patient

Background and Objectives. Epinephrine-containing test doses for detection of intravascular injection during epidural anesthesia may be unreliable or hazardous in beta-blocked, elderly, or pregnant patients. Subtoxic injections of lidocaine have been used as an alternative marker of intravascular injection in unpremedicated patients. We studied two groups of premedicated patients and unpremedicated subjects to evaluate the reliability of the local anesthetics bupivacaine (B) and 2-chloroprocaine (2-CP) as test dose injections. Methods. Thirty ASA I and II subjects received blinded randomized injections of 2-CP, B, or normal saline via a peripheral vein. Results. In group I, 10 healthy unpremedicated volunteers universally recognized injection of 90 mg 2-CP or 25 mg B, but did not reliably detect the injection of 60 mg 2-CP. In group II, 20 patients premedicated with 1 μg/kg fentanyl and 30 μg/kg midazolam could not reliably detect similar injections. Sixteen responded to the injection of 90 mg 2-CP, while 13 detected the 25 mg B test dose. A blinded observer rated only 12 of the subjective reports as conclusive of detection of intravascular injection after each drug. There were no false-positive reports in any group. Conclusions. While 90 mg 2-CP or 25 mg B may be reliable alternatives to epinephrine test doses in unpremedicated subjects, they are unreliable indicators of intravascular injection in the premedicated patient.

The 29th Annual Meeting of SOAP

The 29th Annual Meeting of SOAP

Hemodynamic Responses to an Epinephrine Test Dose in Adults During Epidural or Combined Epidural-General Anesthesia

Hemodynamic Responses to an Epinephrine Test Dose in Adults During Epidural or Combined Epidural-General Anesthesia

The Efficacy of Epinephrine Test Doses During Spinal Anesthesia in Volunteers

The Efficacy of Epinephrine Test Doses During Spinal Anesthesia in Volunteers

Hemodynamic Responses to an Epinephrine Test Dose in Adults During Epidural or Combined Epidural-General Anesthesia

The efficacy of an epinephrine test dose during epidural and combined epidural-general anesthesia is unknown. Thirty-two patients were randomized to receive 2% lidocaine at either a high (25 mL) or low (12 mL) thoracic level of epidural anesthesia followed by general anesthesia with 1 minimum alveolar anesthetic concentration nitrous oxide and isoflurane. A 15-micro gram epinephrine test dose was intravenously administered prior to placement of the lumbar epidural catheter, 20 min after initiation of epidural anesthesia, and after 10 min of stable end-tidal concentrations of general anesthesia. Only high thoracic levels (T-5) of epidural anesthesia reduced the peak systolic blood pressure response to epinephrine (34 +/- 17 vs 18 +/- 11 mm Hg, control versus epidural stage; P < 0.05) and reduced the peak heart rate response when combined with general anesthesia (31 +/- 11 vs 15 +/- 8 bpm; P < 0.05). Incidences of identification of intravascular injection from hemodynamic responses were similarly reduced for systolic blood pressure (100% vs 44%) and heart rate (100% vs 38%). The standard 15-micro gram epinephrine test dose is unaffected by low thoracic levels of epidural anesthesia, but may have decreased sensitivity for detection of intravascular injection during high thoracic levels of epidural anesthesia, especially during general anesthesia. (Anesth Analg 1996;83:97-101)

Hemodynamic Response to an Intravenous Epinephrine Test dose During Combined Spinal/Epidural Anesthesia

Hemodynamic Response to an Intravenous Epinephrine Test dose During Combined Spinal/Epidural Anesthesia

Donʼt Abandon Test Doses

In Response: We believe that Mulroy et al. have misinterpreted our editorial. The editorial and the article [1] that prompted it specifically apply to vascular patients. These patients are at risk for myocardial ischemia or dysfunction with a test dose of epinephrine. In fact, one of the coauthors of the letter (Batra) was an investigator in a study [2] in which electrocardiographic changes were induced with a test dose of 15 micro gram of epinephrine. Of 175 individuals tested with epinephrine, 7 had junctional rhythm; 3, premature ventricular contractions; 2, atrial tachycardia; and almost 50% (82 patients) had either T-wave flattening, T-wave inversion, or ST depression consistent with what we would today call myocardial ischemia. Careful readers of our editorial will find that our intention was not to advocate the abandonment of test doses but to suggest that determining the optimal test dose is inappropriate before a real benefit of a test dose has been shown. Many seemingly logical practices in medicine have proved useless when studied scientifically. For instance, we no longer require that 10 g of hemoglobin be given to "healthy" patients before surgical procedures when blood loss is not expected, or that potassium levels be normal before surgery in asymptomatic patients not receiving digoxin. In the past, these transfusions and potassium treatments may have resulted in more harm than help to patients. Our plea in the editorial was for rigor in using a test dose in patients at risk for complications. Although toxicity may occur from intravascular injection, there are no data to show that adding epinephrine to bupivacaine actually reduces risk or lessens complications. What we meant to communicate in the editorial was, before an optimal test dose of epinephrine is evaluated in vascular surgery patients, the real benefit versus harm of such a test dose must be determined. We should not seek the dose that is least likely to produce tachycardia, but rather a dose not associated with symptoms likely to involve greater risk than benefit. Our response to the letter of Mulroy et al. has given us the opportunity to express the ideas in our editorial more clearly. Alicia Toledano, SCD Joseph Foss, MD Michael F. Roizen, MD Department of Anesthesia and Critical Care University of Chicago Chicago, IL 60637

Epidural Test Dosing

In Response: We wholeheartedly agree with the comments by Dr. Colclough. Our editorial [1] questioned the value of the test dose only in patients subject to high risk of complications from epinephrine, such as patients with vascular disease. Further data are needed to adequately assess the value of an epinephrine test dose in other patient populations. Alicia Toledano, ScD Michael F. Roizen, MD Department of Anesthesia and Critical Care University of Chicago Chicago, IL 60637

When Is Testing the Test Dose the Wrong Thing to Do?

T he article by Schoenwald et al. in this issue (1) is one of many in the anesthesia literature that report on the optimal test dose before epidural anesthesia to determine whether the catheter has been misplaced in a surgical patient. Like the others, this article seems to dismiss an important question: Is a test dose necessary? If so, what are its relative risks and benefits? The benefits and risks for any test must be evaluated, at least theoretically, before we consider the best conditions for performing the test. Let us explore the risks and benefits of test doses in vascular surgical patients to justify the search for an optimal test dose in that population. Epidural catheters can be misplaced into either the intravenous or subarachnoid space. A misplaced catheter can be identified by the return of blood or cerebrospinal fluid spontaneously or with aspiration; by the use of sequential divided doses, rather than a single dose; and by the use of an additional drug, commonly epinephrine, to elicit a physiologic sign of misplacement (2,3). In epidural anesthesia for obstetrics, misplaced catheters not detected by blood return or aspiration and subsequent incremental dosing are very rareless than 1% (4,5). But obstetric patients may belong to a different risk group than vascular patients. In vascular surgery patients, the frequency with which epidural catheters are misplaced, and whether misplacement can be detected by the first two methods described above, is not known. We need more information before we can determine whether a significant problem exists and, if so, whether we should focus on a test dose to solve it. We strongly recommend that prevalence studies be undertaken to quantify the likelihood that a misplaced catheter will remain undetected in vascular surgical patients even after aspiration and sequential dosing. If we find a problem that can be resolved by a test dose, we can assess the value of the test by clinical

Vital Sign Changes to an iv Test Dose of Epinephrine and Lidocaine with and without Glycopyrrolate Pretreatment

In order to decrease complications of local anesthetic, early detection of intravascular injection of local anesthetics is inevitable. However, heart rate response to intravenous(iv) epinephrine test dose injection may result in false-positive or false-negative result. Besides, glycopyrrolate pretreatment may enhance heart rate response to epinephrine test dose. We allocated randomly 30 ASA physical status 1 and 2 patients to two groups, to receive glycopyrrolate 0.2 mg(n=15) or same volume of saline(n=15). Five minutes after glycopyrrolate pretreatment, patients received iv test dose of 2% lidocaine 3 ml with epinephrine 15 pg at a rate of 1 ml/sec. Two groups were similar with respect to basal heart rate. Heart rate and mean arterial pressure increased significantly in both groups at 1, 2, 3 and 4 minutes after epinephrine test dose injection. After 5 minutes, heart rate and mean arterial pressure normalized in both groups. Thus we might suggest that glycopyrrolate pretreatment has no influence on the sensitivity of the test dose containing 2% lidocaine 3 ml and epinephrine 15 μg to detect intravascular injection of local anesthetics.

Sympatho-adrenal stimulation by carbon dioxide and the inhibitory effect of carbonic acid on epinephrine response.

Carbon dioxide serves as a potent stimulus to increase the titer of circulating sympatho-adrenal catechol amines in the cat. Using the denervated nictitating membrane as an assay method the CO2 threshold for adrenal stimulus was determined to be about 15% concentration in alvcolar air. Adrenalectomy decreased by 60% the catechol amine titer initiated by 30% CO2, but hepatectomy was ineffective. The stimulant effect of CO2 in this action was specific and was not dependent on the change in hydrogen ion concentration. The spinal cat was almost as responsive as the normal to CO2 stimulus, but if the cord was destroyed only a very low catechol amine concentration could be detected with comparable stimulus. In the intact cat much of the inhibition of response to administered epinephrine by CO2 is more apparent than real, because the CO2 itself serves as a stimulus to raise the endogeneous epinephrine titer and each subsequently administered test dose of epinephrine was then examined against a background of hormone action. Because of the alinear shape of the epinephrine dose-response curve this can be misinterpreted as ‘inhibition.’ There was however, a direct CO2 inhibition of epinephrine-induced smooth muscle contraction which was most apparent in the range 3–15% alveolar CO2. Sympathetically innervated and denervated structures were inhibited to the same degree.

Enhancement of Epinephrine Induced Cardiac Arrhythmias by Tetraethylammonium Chloride (Etamon).

In the experiments to be reported herein tetraethylammonium chloride has been shown to intensify the cardiac arrhythmias occurring in dogs during cyclopropane anesthesia. Secondly, experiments on unanesthetized animals suggest that the choice of a pressor agent for use as an antidote after tetraethylammonium chloride may be critical. After tetraethylammonium injection epinephrine resulted in ventricular tachycardia whereas phenylephrine (Neo-Synephrine) caused no arrhythmias. Cardiac arrhythmias occurring during cyclopropane anesthesia have been demonstrated experimentally to depend upon reflex sensitization of the heart to epinephrine. Cyclopropane stimulates receptors located in the abdominal viscera, producing afferent impulses which pass to the cord by way of fibers travelling with the splanchnics. The reflex center is located in the brain, presumably in the hypothalamus. Efferent impulses pass to the heart by way of cardiac sympathetics. Since interruption of this pathway at any point has prevented the arrhythmias, the tetraethylammonium ion should theoretically block the reflex sensitization. This agent has been reported to interrupt sympathetic impulses by ganglionic blockade and consequently was expected to block the efferent impulses. When it was found that tetraethylammonium potentiated the cardiac effects of epinephrine under cyclopropane, the cardiac effects of the ion and epinephrine were also investigated in unanesthetized animals. Epinephrine has been recommended as an antidote for the profound hypotension which may follow the clinical administration of tetraethylammonium. Cyclopropane-epinephrine Ventricular tachycardia was produced in the dog by the method described by Meek et al. The only modification of this technic was reduction of the standard test dose of epinephrine in order to lower the mortality from ventricular fibrillation. After the control duration of ventricular tachycardia had been determined, tetraethylammonium chloride was administered intravenously over a period of 60 seconds in doses of 5 to 20 mg/kg.

Effects of Dibenamine on Cardiovascular Actions of Epinephrine, Acetylcholine, Pitressin and Angiotonin in Unanesthetized Dogs.

Summary and ConclusionsThe actions of Dibenamine on the cardiovascular adjustments caused by epinephrine, acetylcholine, pitressin, and angiotonin have been studied in unanesthetized dogs. Dibenamine produced an increase in heart rate which persisted for one to 3 hours.A test dose of epinephrine which regularly caused reflex cardiac slowing in normal unanesthetized dogs produced severe cardiac acceleration after administration of Dibenamine. This acceleration is attributable to the direct stimulatory action of epinephrine on the sino-auricular node and to reflex acceleration from a fall in blood pressure.The compensatory cardiac acceleration produced by injection of a test dose of acetylcholine was undiminished and prolonged in unanesthetized animals under the influence of Dibenamine. This result is compatible with the interpretation that the vasoconstrictor mechanisms are impaired while the cardioaccelerator mechanisms are relatively intact.The severe cardiac inhibition produced by pitressin and angioton...

Protecting Action of Chemicals Related to Procaine on Ventricular Fibrillation During Cyclopropane Anesthesia

ConclusionsThe administration of p-amino benzoic acid, the calcium double salt of benzyl succinic and p-amino benzoic acids, or sodium p-amino benzoate prior to a test dose of epinephrine during cyclopropane anesthesia reduced the incidence of ventricular fibrillation. The intracardiac injection of procaine at the time when ventricular fibrillation developed effected a return to normal in a number of cases. Ventricular fibrillation was not ameliorated by the intracardiac injection of the other three p-amino benzoic acid derivatives.The authors wish to express their appreciation for the helpful suggestions of Dr. Arthur C. DeGraff.

Protecting Action of Procaine Against Ventricular Fibrillation Induced by Epinephrine During Cyclopropane Anesthesia

ConclusionsThe experiments presented support the contention that when procaine is administered to cyclopropanized dogs the incidence of ventricular fibrillation following epinephrine administration is reduced. Sixty percent of the animals developed ventricular fibrillation after injection of one test dose of epinephrine. When procaine was previously administered all animals were protected, and the introduction of 8 test doses of epinephrine were required to produce the fatal complication. The results also indicate that procaine may be efficient in the treatment of ventricular fibrillation induced in the dog by epinephrine during cyclopropane anesthesia. In every instance in which procaine was given intravenously at the time when ventricular tachycardia occurred following the administration of epinephrine, recovery was effected.