Search

Background: Application of positive end-expiratory pressure (PEEP) has been used to increase the cross-sectional area (CSA) of the right internal jugular vein (IJV) in order to facilitate catheterisation. We aimed to determine the PEEP level at which the maximum increase of CSA occurred., Methods: We enrolled 60 American Society of Anesthesiologists physical status I and II patients undergoing general endotracheal anaesthesia. The CSA was measured in the supine position with no PEEP (control condition, P0) and after applying five different PEEPs in random order: 3 (P3), 6 (P6), 9 (P9), 12 (P12), and 15 (P15) cm H(2) O. Ultrasound was used to measure and record the CSA of the right IJV at the level of the cricoid cartilage., Results: All PEEP levels increased the CSA of the right IJV relative to the control (all P < 0.05). On average, P3, P6, P9, P12, and P15 increased the CSA by 21.5, 37.4, 51.9, 66.5, and 72.4%, respectively. There was no significant increase in CSA above a PEEP of 12 cm H(2) O., Conclusion: The application of PEEP effectively increases the CSA of the right IJV. The PEEP giving the largest CSA is 12 cm H(2) O., (© 2012 The Authors. Acta Anaesthesiologica Scandinavica © 2012 The Acta Anaesthesiologica Scandinavica Foundation.)

Background: We hypothesized that the administration of ephedrine and phenylephrine for maternal hypotension modifies cardiovascular hemodynamics in near-term sheep fetuses., Methods: At 115-136 days of gestation, chronically instrumented, anesthetized ewes with either normal placental function or increased placental vascular resistance after placental embolization were randomized to receive boluses of ephedrine (n = 12) or phenylephrine (n = 12) for epidural-induced hypotension after a short period of hypoxemia. Fetal cardiovascular hemodynamics were assessed by Doppler ultrasonography at baseline, during hypotension and after vasopressor treatment., Results: During hypotension, fetal PO(2) decreased and proximal branch pulmonary arterial and pulmonary venous vascular impedances increased. Additionally, in the embolized fetuses, the time-velocity integral ratio between the antegrade and retrograde blood flow components of the aortic isthmus decreased. These parameters were restored to baseline conditions by ephedrine but not by phenylephrine. With phenylephrine, weight-indexed left ventricular cardiac output and ejection force decreased in the non-embolized fetuses, and the proportion of isovolumetric contraction time of the total cardiac cycle was elevated in the embolized fetuses., Conclusions: After exposure to hypoxemia and maternal hypotension, ephedrine restored all fetal cardiovascular hemodynamic parameters to baseline. Phenylephrine did not reverse fetal pulmonary vasoconstriction or the relative decrease in the net forward flow through the aortic isthmus observed in fetuses with increased placental vascular resistance. Moreover, fetal left ventricular function was impaired during phenylephrine administration.

Background: Onset of action of muscle relaxants is influenced by cardiac output and muscle blood flow. Ephedrine reduces the onset time of rocuronium. Onset is also shortened by priming. Accordingly, we hypothesized that priming combined with ephedrine is superior to either technique used separately., Methods: Four groups of randomly allocated patients (n = 31), ASA I - II, were induced with propofol 2.5 mg kg(-1). In groups I and II, 0.04 mg kg(-1) of rocuronium was followed by a 3-min priming interval. Induction was followed by an intubation dose of 0.04 mg kg(-1). Then a 30-s intubation was attempted. In groups III and IV the same sequence was repeated except for sham priming and an intubation dose of 0.44 mg kg(-1). In groups I and II, ephedrine (210 microg kg(-1)) was injected before propofol. In groups II and V, an equivalent volume of normal saline was injected. Jaw relaxation, vocal cord position, and diaphragmatic response were used to assess intubating conditions., Results: All patients of group I were intubated 30 s after the intubating dose and within a 20-s interval compared with 74% of patients in groups II and III, and 84% of patients in group IV. Intubating conditions were graded good to excellent in all patients in group I compared with 42% of those in group II, 35% in group III and 52% in group IV (P < 0.01 vs. group I). During the priming interval, no adverse effects were observed or reported., Conclusions: Ephedrine in combination with propofol significantly improved clinical intubating conditions at 30 s following priming with rocuronium compared with priming with ephedrine without priming.

Background: The aim of this study was to evaluate the effect of ephedrine administered prior to induction of anaesthesia on the onset time of succinylcholine for endotracheal intubation., Methods: Patients were randomly assigned to receive intravenously (i.v.) either 70 microg kg(-1) of ephedrine (Group I; n = 25) or saline (Group II; n = 25) 3 min before induction of anaesthesia. Induction of anaesthesia was provided with propofol 2 mg kg(-1) plus remifentanil 1 microg kg(-1). Onset time and duration of muscle fasciculation and onset time of succinylcholine were recorded. Intubation was attempted after establishment of 100% thumb relaxation and difficulties were recorded. Heart rate, pulse oxymetry (SpO2) and mean arterial pressure (MAP) were also recorded., Results: The onset time of succinylcholine were significantly (P < 0.001) shorter in Group I (26 +/- 4 s), when compared with Group II (43 +/- 6 s). Patients in Group I were intubated at 49 +/- 7 s compared with 68 +/- 10 s in Group II. The score of intubation was similar in both groups. Duration of muscle fasciculation was longer in Group II. Heart rate and MAP increased significantly (P < 0.05) after ephedrine injection, compared with the baseline value in Group I., Conclusions: The onset time of succinylcholine can be shortened with ephedrine pretreatment.

Background: We investigated the hypothesis that manipulation of cardiac output (CO) with esmolol (Es) or ephedrine (E) affects the onset time of rocuronium., Methods: Following anesthesia induction, 33 patients received E (70 micro g kg-1), Es (500 micro g kg-1) or placebo (P) 30 s before rocuronium (0.6 mg kg-1) administration. Cardiac output was measured non-invasively after intubation every 3 min. The interval from the end of rocuronium administration to the disappearance of all twitches was considered to be the onset time., Results: Onset time was shorter after E (52.2 +/- 16.5 s) and longer after Es (114.3 +/- 11.1 s) compared with P (87.4 +/- 7.3 s) (P < 0.0001). Cardiac output increased (P < 0.05) in group E for 15 min after rocuronium. In group Es, CO decreased (P < 0.05) at 3 and 6 min. Cardiac output was higher in group E vs. group Es, 3-6 min post administration of rocuronium (P=0.015)., Conclusion: Pretreatment with E or Es appears to affect the onset time of rocuronium by altering CO as measured with the NICO (Non-Invasive Cardiac Output) monitor (Novametrix Medical Systems Inc., Willingford, CO).

Background: Ephedrine is one of the most commonly used non-catecholamine sympathomimetic agents. It is used in operating rooms and critical care settings worldwide. While it has many side effects, its ability to rapidly raise blood pressure makes it an ideal agent to maintain homeostasis as well as in emergency situations. While its effects are known to be mediated by an alpha-mediated mechanism, the exact alpha subtype is unknown. In addition, no studies using ephedrine have been performed in the pulmonary vascular bed of the cat., Methods: The effects of phentolamine, a non-selective alpha-receptor blocker, and prazosin, an alpha1-selective antagonist, were investigated on pulmonary arterial responses to ephedrine, phenylepherine, norepinephrine, and U-46619. Lobar arterial perfusion pressure was continuously monitored, electronically averaged, and recorded with constant flow in the isolated left lower lobe vascular bed of the cat., Results: Phentolamine and prazosin significantly reduced vasoconstrictor pulmonary perfusion pressure increases induced by ephedrine., Conclusion: Ephedrine has significant vasopressor activity in the pulmonary vascular bed of the cat meditated predominantly by alpha1 adrenergic receptor activation.

Bolus doses of ephedrine are often used by anaesthesiologists for intraoperative hypotension. This randomized single-blind cross-over study was designed to simultaneously evaluate circulatory, respiratory and metabolic effects of intravenously given ephedrine in 12 healthy male volunteers. Oxygen uptake and carbon dioxide excretion were measured with indirect calorimetry and non-invasive transthoracic electrical bioimpedance was used for cardiac output measurements. The maximum effect on most variables was reached at 4-5 min. At 5 min after the administration of ephedrine 0.1 mg per kilogram body weight, there were significant increases in cardiac index, systolic and mean arterial blood pressure, expired minute volume, oxygen uptake and carbon dioxide excretion rates. There were no significant changes in the quotient between oxygen uptake rate and cardiac index, VO2/CI during the 30 min study period. The O2 saturation was not altered. The present study indicates that ephedrine increases oxygen demand and supply in a similar magnitude.

Morphine-ephedrine interaction on analgesia was studied in mice (n = 240) and in post-operative patients (n = 32). It was found that combining morphine and ephedrine enhances analgesia which is not significantly different from the effect of morphine given alone at double dose.

The effects of ephedrine and phenylephrine on fetal and maternal plasma atrial natriuretic peptide (ANP) concentrations were studied during 30 elective cesarean sections. After induction of spinal anesthesia, reductions from baseline maternal blood pressure were corrected with one of these pressor agents administered in a double-blinded, randomized manner. Immediately following delivery, umbilical artery (UA) ANP concentrations were significantly higher than umbilical vein (UV) concentrations (pg/ml) for both groups (ephedrine, 120.8 +/- 64.0 vs. 86.8 +/- 40.8, phenylephrine, 125.0 +/- 54.2 vs. 72.4 +/- 31.7), but there were no differences between groups for UA and UV ANP levels. Postpartum maternal ANP concentrations were significantly higher than baseline values in both groups, but again there were no differences between groups. Correlations between total doses of ephedrine or phenylephrine and UA or UV ANP levels did not reach significance. Postpartum maternal (MV2), UA, and UV blood gas variables (pH, PCO2, and PO2) were also not different between groups. These data suggest that effects of pressor doses of ephedrine (beta and alpha agonist) and phenylephrine (alpha agonist) on maternal and fetal ANP levels are not different. Therefore, 1) assuming these pressor drugs stimulate ANP release, this stimulation is not solely mediated by beta receptors and 2) to the extent that fetal ANP influences feto-placental circulatory homeostasis, the effects of ephedrine and phenylephrine on this regulatory mechanism do not appear to be different.

Combined effects of adrenergic and intravenous anesthetic agents on phosphatidylinositol (PI) turnover were studied using rat liver prisms incubated with [3H]myo-inositol. Rat liver prisms responded to epinephrine, norepinephrine and phenylephrine dose-dependently with an increase in inositol monophosphate (IP1) formation but they did not respond to ephedrine. Dopamine-induced effects were seen only at concentrations as high as 10(-4) mol.l-1. The enhancement of IP1 formation induced by epinephrine was potentiated by thiamylal at concentrations of 10(-5) mol.l-1 and 10(-4) mol.l-1, remained unaffected by ketamine, fentanyl or midazolam, but was dose-dependently inhibited by droperidol. The present results from in vitro studies of liver cell metabolism suggest that alpha-adrenergic agents in combination with barbiturates may potentiate liver cell damage by activation of PI turnover and interrelated intracellular Ca++ accumulation.

The purpose of this study was to assess the risk of alcohol-induced hypoglycaemia from the use of irrigating fluids containing ethanol in transurethral surgery. In the first part of the study, seven healthy male volunteers, aged between 26 and 36, received 1000 ml of irrigating fluid by intravenous infusion. The results confirm the existence of an alcohol-induced decrease in blood glucose when ethanol is given together with 1.5% glycine. In the second part of the study, 40 patients, between 56 and 88 years of age, underwent epidural anaesthesia and a transurethral resection of the prostate (TURP) in which the irrigating fluid used contained 1.5% glycine and either 1% or 2% ethanol. The results suggest that the use of ethanol-containing irrigating fluids is often followed by a slight reduction of the blood glucose level, but the magnitude of this change is too small to be of clinical importance.

The short-term effect of epidural anaesthesia (EDA) on the serum potassium (S-K) concentration was studied in 40 elderly men scheduled for minor urological surgery. In Group I, EDA was induced with mepivacaine 2% + adrenaline 1:200,000 (n = 20) and in Group II mepivacaine 2% was used (n = 20). When EDA had been induced, the mean plasma level of adrenaline was tripled in Group I, while it had decreased in Group II. In Group I there was a decrease in the arterial S-K concentration of up to 0.75 mmol.l-1 with a mean of 0.31 mmol.l-1, s.d. 0.20 (P less than 0.001). In Group II, a small but significant decrease of the S-K level was recorded in arterial (0.14 mmol.l-1, s.d. 0.14; P less than 0.001) but not in venous serum. Two-way analysis of variance showed that the addition of adrenaline to the local anaesthetic solution, but not the choice of using arterial or venous serum for analysis, significantly correlated to the lowering of the S-K concentration (P less than 0.001).

Atrial natriuretic peptide (ANP) is stored in the atrial cardiocyte and is capable of exerting potent, selective, and transient effects on fluid and electrolyte balance and on blood pressure. Because fluid shifts and hemodynamic adjustments occur during parturition, ANP might play a homeostatic role in the parturient and fetoplacental unit. We measured maternal and fetal plasma ANP concentrations in 19 parturients during elective caesarean section. Plasma ANP levels were also measured in seven nonpregnant women of the same age group. The baseline ANP concentration in parturients was significantly higher (29.77 +/- 6.06 pg/ml vs 7.37 +/- 2.1 pg/ml; mean +/- s.e.mean) than in their nonpregnant counterparts. The umbilical artery (UA) ANP concentration was significantly higher than the umbilical vein concentration (91.91 +/- 14.91 pg/ml vs. 40.04 +/- 9.71 pg/ml). Factors under the anaesthesiologist's control may influence maternal and fetal plasma ANP levels. There was a significant correlation between the volume of maternal Ringer's lactate infusion received and maternal ANP concentration. A significant correlation was seen between the total dose of ephedrine administered acutely prior to delivery and the UA ANP concentration. These data suggest that: 1) increased blood volume during pregnancy is associated with increased maternal plasma ANP levels, and 2) the fetus can produce its own ANP, and is thereby capable of responding to ANP stimulating factors.

High lumbar epidural block was induced in seven dogs with 0.5% bupivacaine, causing a fall in mean arterial blood pressure (AP) from 19.2 +/- 3.2 to 10.5 +/- 3.2 kPa, owing to equal reductions in cardiac output (QT) and systemic vascular resistance (SVR). After the administration of ephedrine (a single injection of 200-300 micrograms X kg-1 b.w. followed by a continuous infusion of 10-20 micrograms X kg-1 b.w. X min-1) AP, QT and SVR rose to pre-epidural values. Furthermore, the hypokinetic circulation following the epidural block returned to normokinetic levels. Portal venous blood flow was increased from 16.5 +/- 6.2 to 25.5 +/- 4.3 ml X kg-1 b.w. X min-1 by ephedrine, while the hepatic arterial blood flow was unchanged and remained at its pre-epidural level. In spite of a slight rise in hepatic oxygen consumption from 1.2 +/- 0.4 to 1.6 +/- 0.6 ml X kg-1 b.w. X min-1, the percentages of oxygen extracted from the portal vein and the hepatic artery decreased significantly. It is concluded that ephedrine restores central and splanchnic haemodynamics in a desirable manner during high epidural anaesthesia.

The effects of a 20 mg i.v. bolus of ephedrine sulphate on haemodynamics and plasma lidocaine concentrations were evaluated in eight volunteer subjects receiving a constant i.v. infusion of lidocaine HC1 (2 or 4 mg-min-1). Injection of ephedrine caused a significant increase in mean arterial blood pressure, which preceded an elevation of heart rate by about 2 min. Cardiac output and hepatic blood flow, measured at 10 and 20 min after injection, were also increased significantly, while there was a decrease in total peripheral resistance and no change in splanchnic vascular resistance. There were no significant circulatory alterations over the same period in a control group of four subjects on receiving the lidocaine infusion. After ephedrine, the mean splanchnic extraction ratio of lidocaine fell from 0.76 to 0.66 at 10 min, then rose again to 0.71 at 20 min, and these changes were accompanied by a 9% increase in its splanchnic clearance. Extraction and clearance remained unchanged in the control group. The implications of these findings are considered in relation to the use of ephedrine to prevent or treat hypotension after peridural block with local anaesthetic agents.

The haemodynamic and renal effects of ephedrine were studied in 11 mechanically ventilated patients on the first day after major vascular surgery. Ephedrine, a sympathomimetic agent with alpha-1, beta-1, and beta-2 agonistic activity, was infused into 11 patients to achieve a 20% rise in systolic blood pressure. The doses used were 2-6 micrograms/kg/min, and in six of these 11 patients the dose was then doubled, 4-12 micrograms/kg/min for another renal function test. Blood pressure, heart rate, and cardiac output increased at both dose-ranges. Systolic pulmonary arterial pressure increased by 10% at the first dose-range. Systemic vascular resistance was unchanged and plasma catecholamine levels were unaltered in the present study. Plasma renin activity diminished by 18% and 6%, respectively. Clearance of para-aminohippuric acid increased by 20% and 6%, at the two dose-ranges, while clearance of inulin and urine flow rate increased by 24% and 29%, respectively, at the first dose-range, without further increase during the second dose-range. Fractional chloride excretion, and fractional osmolar clearance were unaltered. Fractional Na+ clearance rose by 30% and 36%, respectively. Fractional free water clearance diminished by 8% at the second dose-range. When comparing the two dose-ranges, HR, systolic and mean BP rose by 8%, 13% and 11%, respectively. Fractional K+ excretion diminished by 30%. We conclude that ephedrine given as a continuous infusion seems to have beneficial effects on renal function in patients after elective major vascular surgery.