Blake Dw

Prospective randomized trial of high thoracic epidural analgesia for coronary artery bypass surgery

BACKGROUND Postoperative pain may be severe after coronary artery bypass surgery. High thoracic epidural analgesia (HTEA) provides intense analgesia. METHODS Eighty patients were randomized to HTEA or intravenous morphine analgesia (control). Patients received coronary artery bypass surgery (CABG) with cardiopulmonary bypass. Pain was measured by visual analogue scale 0 to 10. Psychologic morbidity, intraoperative hemodynamics, ventricular function, lung function, and physiotherapy cooperation were also assessed. On the third postoperative day HTEA and morphine were ceased and only oral medications were used. Acetaminophen, indomethacin, and tramadol were allowed as supplemental analgesics in both groups. RESULTS The primary endpoint of pain scores was significantly less with HTEA on postoperative days 1 and 2 at rest, 0.02 +/- 0.2 versus 0.8 +/- 1.8 (p = 0.008) and 0.1 +/- 0.4 versus 1.2 +/- 2.7 (p = 0.022), respectively, and with coughing 1.2 +/- 1.7 versus 4.4 +/- 3.1 (p < 0.001) and 1.5 +/- 2.0 versus 3.6 +/- 3.1 (p = 0.001), respectively. When HTEA and morphine were ceased on day 3, there were no significant differences. The secondary endpoints of postoperative depression (p = 0.033) and posttraumatic stress subscales (p = 0.021) of the Minnesota Multiphasic Personality Inventory were lower with HTEA. Extubation occurred earlier with HTEA, 2.6 versus 5.4 hours (p < 0.001). HTEA showed improved physiotherapy cooperation (p < 0.001), arterial oxygen tension (p = 0.041), and peak expiratory flow rate (p = 0.001). Mean arterial pressure was lower with HTEA (p = 0.036), otherwise there were no differences in intraoperative hemodynamics or ventricular function. CONCLUSIONS Epidural analgesia reduces pain after coronary operation and is associated with improved physiotherapy cooperation, earlier extubation, and reduced risk of depression and posttraumatic stress.

A Comparison of Epidural Ropivacaine Infusion Alone and in Combination with 1, 2, and 4 [micro sign]g/mL Fentanyl for Seventy-Two Hours of Postoperative Analgesia After Major Abdominal Surgery

UNLABELLED Our aim in this prospective, randomized, double-blinded study was to compare the analgesic effectiveness and side effects of epidural infusions with ropivacaine 2 mg/mL alone (Group R; n = 60) and in combination with fentanyl 1 microg/mL (R1F; n = 59), 2 microg/mL (R2F; n = 62), and 4 microg/mL (R4F; n = 63) for up to 72 h after major abdominal surgery. Effective epidural neural blockade was established before surgery; postoperatively, the infusion rate was titrated to a maximum of 14 mL/h for analgesia. No additional analgesics other than acetaminophen were permitted during the infusion. The median of individual visual analog scale score with coughing were <20 mm for all groups (0 = no pain, 100 = worst pain) and was significantly lower (P < 0.01) for Group R4F at rest and with coughing (compared with Group R). Infusions were discontinued due to inability to control pain in significantly fewer patients in Group R4F (16%) than the other groups (34% to 39%; P < 0.01). For all groups, >90% of patients had no detectable motor block after 24 h. Hypotension, nausea, and pruritus were more common with the larger dose of fentanyl. We conclude that, after major abdominal surgery, an epidural infusion of ropivacaine 2 mg/mL with fentanyl 4 microg/mL provided significantly more effective pain relief over a 3-day period than ropivacaine alone or ropivacaine with lower concentrations of fentanyl. IMPLICATIONS Postoperative epidural analgesic infusions are widely used, but there is little information regarding optimal strengths of opioid with local anesthetic. In this blinded, prospective study, we compared four different epidural infusion solutions for efficacy and side effects over a clinically useful postoperative period and conclude that an epidural infusion of ropivacaine 2 mg/mL with fentanyl 4 microg/mL was most effective.

The effects of cardiopulmonary bypass on total and unbound plasma concentrations of propofol and midazolam.

OBJECTIVE To examine the effects of cardiopulmonary bypass (CPB) on total and unbound plasma concentrations of propofol and midazolam when administered by continuous infusion during cardiac surgery. DESIGN Prospective clinical study. SETTING University hospital. PARTICIPANTS Twenty-four adult patients undergoing cardiac surgery. INTERVENTIONS Patients received either propofol or midazolam to supplement fentanyl anesthesia. Twelve patients received a propofol bolus (1 mg/kg) followed by an infusion of 3 mg/kg/hr. A second group received midazolam, 0.2 mg/kg bolus, followed by an infusion of 0.07 mg/kg/hr. MEASUREMENTS AND MAIN RESULTS Blood sample were collected from the radial artery cannula at 0, 2, 4, 8, 8, 10, 15, 20 minutes and then every 10 minutes before CPB, at 1, 2, 3, 4, 6, 10, 15, 20 minutes and then each 10 minutes during CPB. On weaning from CPB samples were collected at 0, 5, 10 and 20 minutes. Plasma binding, total and unbound propofol and midazolam concentrations were determined by ultrafiltration and high-pressure liquid chromatography (HPLC). CPB resulted in a fall in total propofol and midazolam plasma concentrations, but the unbound concentrations remained stable. The propofol unbound fraction increased from 0.22 +/- 0.06% to 0.41 +/- 0.17%. The midazolam unbound fraction increased from 5.6 +/- 1.0% to 11.2 +/- 2.1%. CONCLUSIONS Unbound concentrations of propofol and midazolam are not affected by cardiopulmonary bypass. Total intravenous anesthesia algorithms do not need to be changed to achieve stable unbound plasma concentrations when initiating CPB.

INTERACTIONS BETWEEN THE CIRCULATORY EFFECTS OF CENTRAL HYPOVOLAEMIA AND ARTERIAL HYPOXIA IN CONSCIOUS RABBITS

1. Eight conscious rabbits were repeatedly subjected to progressive reduction in central blood volume by gradually inflating a thoracic inferior vena caval‐cuff so cardiac index (CI) fell at a constant 8.5% of baseline/min.

Correction of hypovolemic hypotension by centrally administered naloxone in conscious rabbits

Our goal was to test directly whether the vasoconstrictor action of naloxone during hypovolemic hypotension is centrally mediated. In eight chronically instrumented rabbits, progressive central hypovolemia and fall in cardiac output (CO) were produced by gradually inflating a cuff on the thoracic vena cava. Central hypovolemia was then sustained for 8 min by holding CO constant. In the main experiment (n = 4), each rabbit was studied eight times over 4 experimental days. Saline or naloxone treatment commenced 10 min before progressive hypovolemia (early treatment) or 2 min after the onset of sustained hypovolemia (late treatment), given by intravenous infusion or into the fourth ventricle (V4). With saline treatment, there was spontaneous recovery of systemic vasoconstriction and arterial pressure during sustained hypovolemia. Late treatment with naloxone (4 mg/kg i.v.; 4-37 micrograms/kg V4) accelerated and exaggerated these changes. Thus, under conditions of constant CO and central blood volume, the vasodilatation of the decompensatory phase of acute hypovolemia is not sustained, and intravenous nalox ones vasoconstrictor action is via a brain stem mechanism.Our goal was to test directly whether the vasoconstrictor action of naloxone during hypovolemic hypotension is centrally mediated. In eight chronically instrumented rabbits, progressive central hypovolemia and fall in cardiac output (CO) were produced by gradually inflating a cuff on the thoracic vena cava. Central hypovolemia was then sustained for 8 min by holding CO constant. In the main experiment ( n = 4), each rabbit was studied eight times over 4 experimental days. Saline or naloxone treatment commenced 10 min before progressive hypovolemia (early treatment) or 2 min after the onset of sustained hypovolemia (late treatment), given by intravenous infusion or into the fourth ventricle (V4). With saline treatment, there was spontaneous recovery of systemic vasoconstriction and arterial pressure during sustained hypovolemia. Late treatment with naloxone (4 mg/kg iv; 4-37 μg/kg V4) accelerated and exaggerated these changes. Thus, under conditions of constant CO and central blood volume, the vasodilatation of the decompensatory phase of acute hypovolemia is not sustained, and intravenous naloxones vasoconstrictor action is via a brain stem mechanism.

Cardiovascular reflex responses after intrathecal ω-conotoxins or dexmedetomidine in the rabbit

1. The effects of thoracic intrathecal doses (1 µg/kg) of the α2‐adrenoceptor agonist dexmedetomidine and ω‐conotoxins MVIIA and CVID on vasoconstrictor and heart rate responses to acute central hypovolaemia were studied in seven chronically instrumented rabbits.

Effect Of Amlodipine On Cardiopulmonary Performance In Volunteers

1. In order to exclude a significant effect of the calcium channel antagonist amlodipine on cardiopulmonary performance in normal subjects, we performed a double‐blind cross‐over study of amlodipine (10 mg daily for 2 weeks) on oxygen uptake and catecholamine responses during exercise in eight volunteers.