Biomedical subjects

Russell E Anderson

Publications and source records attributed to Russell E Anderson.

6 recordsLinked to original sources

PubMed2006

Wedging the pulmonary artery catheter: changes in left atrial and pulmonary artery pressures and risk for perforation.

OBJECTIVE: Clinical and experimental data indicate that when there is lung disease, wedging the pulmonary artery catheter (PAC) could cause decreases in cardiac output and systemic arterial blood pressure and an increase in mean pulmonary artery pressure (PAP). The authors studied whether wedging would alter mean left atrial pressure (LAP), and report perforations with PACs in their unit since 1975. DESIGN: Observational study. SETTING: University hospital operating room and intensive care unit. PARTICIPANTS: Ten adult patients undergoing cardiac surgery. INTERVENTIONS: Placement of epidural catheters in the left atrium and pulmonary artery, and a PAC. MEASUREMENTS AND MAIN RESULTS: After weaning from cardiopulmonary bypass, mean LAP, mean PAP, and cardiac output were measured before and during wedging with the chest open and closed. Mean LAP decreased during wedging, from 13.5 +/- 2.8 (SD) mmHg to 13.0 +/- 3.0 mmHg (open chest) and from 15.8 +/- 3.2 mmHg to 15.3 +/- 3.1 mmHg (closed chest; p < 0.001), and mean PAP increased, from 18.8 +/- 3.5 mmHg to 19.7 +/- 3.5 mmHg (open chest) and from 21.3 +/- 4.3 mmHg to 21.9 +/- 4.2 mmHg (closed chest; p < 0.001). Mean PAP-mean LAP increased by 20% to 25%. Wedge pressure did not differ from mean LAP. Cardiac output and systemic arterial pressure did not change. Four perforations due to PACs occurred since 1975. CONCLUSIONS: In adult patients undergoing cardiac surgery, wedging of a PAC resulted in a small decrease in mean LAP and a small increase in mean PAP. The wedging maneuver carries a small risk. How wedging is performed could influence the risk for perforation.

Adult↗

PubMed2005

The postoperative analgesic effects of intra-articular levobupivacaine in elective day-case arthroscopy of the knee: a prospective, randomized, double-blind clinical study.

PURPOSE: Pain and emesis are the two major complaints after day surgery. Local anesthesia has become an important part of optimizing perioperative pain treatment. The aim of the present study was to study two different concentrations of levobupivacaine's effect on postoperative pain following elective arthroscopy of the knee with lidocaine 10 mg/ml with adrenaline as active control. TYPE OF STUDY: Prospective, randomized double-blind study with lidocaine as active control but without placebo. METHODS: One hundred and twenty patients were studied comparing levobupivacaine 2.5 mg/ml, levobupivacaine 5 mg/ml, and lidocaine 10 mg/ml with adrenaline given intra-articularly at the end of day-case operative elective arthroscopy of the knee done in light general anesthesia. Primary study endpoint was the need for any analgesics during the first 24 postoperative hours. RESULTS: Levobupivacaine 5 mg/ml was associated with a reduced need for any analgesia during the entire 24-h study period (p = 0.013) as compared to both 2.5 mg/ml levobupivacaine and lidocaine with adrenaline. Levobupivacine 2.5 mg/ml was inferior to lidocaine with regard to pain relief with an increase in need for oral analgesia already during stay in the recovery unit (p < 0.001). CONCLUSIONS: Levobupivacaine 5 mg/ml was found to be an effective local anesthetic in day-case operative arthroscopy of the knee providing superior postoperative analgesia as compared to lidocaine with adrenaline or a lower concentration of levobupivacaine. LEVEL OF EVIDENCE: Level I: Prospective, randomized double-blind study without placebo.

Ambulatory Care↗

PubMed2005

Effects of cardiopulmonary bypass on glucose homeostasis after coronary artery bypass surgery.

OBJECTIVE: Hyperglycaemia is associated with increased mortality and morbidity after cardiac surgery. While surgical stress results in hyperglycaemia after all operations, it has been suggested that cardiopulmonary bypass is the dominating contributor after cardiac surgery. This study aimed to determine the contribution of cardiopulmonary bypass to hyperglycaemia after coronary artery bypass. METHODS: Patients scheduled for primary coronary artery bypass grafting were randomised to surgery with or without cardiopulmonary bypass. All patients received continuous insulin infusions during the initial 24-h period. Glucose was infused (100mg/kg per h) postoperatively in the intensive care unit but not during surgery. Blood glucose was measured 4 times daily until the third postoperative day. Serum insulin, insulin-like growth factor-1 and its binding protein were determined. RESULTS: Average blood glucose during the day of surgery did not differ between groups, but 30% more insulin (P=0.003) was required when cardiopulmonary bypass was used. Blood glucose 2-3h after meals was higher in patients using cardiopulmonary bypass during the first 3 postoperative days. Fasting blood glucose was still equally elevated 20-30% in both groups on the third postoperative day. Insulin-like growth factor-1 decreased more (P=0.01) and insulin-like growth factor binding protein-1 increased more (P<0.001) with cardiopulmonary bypass than without. The ratio of insulin-like growth factor-1 concentration to the concentration of its binding protein-1 was more negative (indicating greater catabolism) with cardiopulmonary bypass than without both postoperatively (P=0.002) and on the third postoperative day (P=0.02). Insulin-like growth factor-1 standard deviation score, also a measure of catabolism, was greater after surgery with cardiopulmonary bypass than without (P=0.02). CONCLUSIONS: Glucose homeostasis is disturbed preoperatively for many non-diabetic patients undergoing coronary bypass surgery. Cardiopulmonary bypass exacerbates the catabolism and disturbed glucose homeostasis that is induced also to a lesser degree by surgery without cardiopulmonary bypass.

Aged↗

PubMed2003

Biochemical markers of cerebrospinal ischemia after repair of aneurysms of the descending and thoracoabdominal aorta.

OBJECTIVE: To investigate the clinical potential of several markers of spinal cord ischemia in cerebrospinal fluid (CSF) and serum during aneurysm repair of the descending thoracic or thoracoabdominal aorta. DESIGN: Observational study of consecutive patients. Nonblinded, nonrandomized. SETTING: University hospital thoracic surgical unit. PARTICIPANTS: Eleven consecutive elective patients. INTERVENTIONS: Distal extracorporeal circulation and maintenance of CSF pressure <10 mmHg until intrathecal catheter removal. MEASUREMENTS AND MAIN RESULTS: CSF and serum levels of S100B (and its isoforms S100A1B and S100BB), neuronal-specific enolase (NSE), and the CSF levels of glial fibrillary acidic protein (GFAp) and lactate were determined. Two patients had postoperative neurologic deficit. One with a stroke showed a 540-fold increased GFAp, a 6-fold NSE, and S100B increase in CSF. One with paraplegia had a 270-fold increase in GFAp, a 2-fold increase in NSE, and 5-fold increased S100B in CSF. One patient without deficit increased GFAp 10-fold, NSE 4-fold, and S100B 23-fold in CSF. CSF lactate increased >50% in 6 of 9 patients without neurologic deficit. Serum S100B increased within 1 hour of surgery in all patients without any concomitant increase in CSF. S100A1B was about 70% of total S100B in both serum and CSF in patients with or without neurologic defects. S100B in CSF increased 3-fold in 3 of 9 asymptomatic patients. CONCLUSIONS: In patients with neurologic deficit, GFAp in CSF showed the most pronounced increase. Biochemical markers in CSF may increase without neurologic symptoms. There is a significant increase in serum S100B from surgical trauma alone without any increase in CSF.

Adult↗

PubMed2002

Correlation beween AAI-index and the BIS-index during propofol hypnosis: a clinical study.

OBJECTIVE: To determine the degree of linearity and correlation between the anaesthetic depth indices BIS and AAI over a wide range of hypnotic depth using propofol. METHODS: 20 ASA I patients were studied during propofol induction. Co-induction with 0.05 mg fentanyl and 30 mg propofol iv before initiation of the study. Thereafter repeated doses of propofol 0.5 mg/kg iv. every minute until BIS < 30. Loss of responsiveness to verbal command was determined by repeated loud commands to the patient. BIS (Aspect 2000 XP, BIS algorithm 4.0, system rev. 3.12, Aspect Medical Systems; Natick, MA, U.S.A.) and AAI-index (A-Line Auditory Evoked Potential Monitor, version 1.4, Danmeter A/S; Odense, Denmark) were determined simultaneously (n = 15). BIS alone without acoustical stimulation was studied in a control group (n = 5). MAIN RESULTS: Both indices decreased with increasing dose, and there was a high correlation between the two (r2 = 0.82). The indices showed however different values and while BIS were quite linear, the AAI-index had a more on-offb ehaviour. CONCLUSION: The AAI-index correlates with the BIS-index during propofol hypnosis in the absence of surgical stimulation. Neither the BIS-index, heart rate, nor systemic blood pressure were influenced by the acoustical stimulation from the A-line monitor. Both indices decreased in relation to increasing doses of propofol, but the AAI-index was lower both before becoming unconscious, during transition to unconsciousness, and during the deeper levels of sedation. The AAI-index lacks linearity at both very low and higher levels of propofol sedation with a nearly on-off behaviour for wakefulness vs hypnosis.

Adult↗

PubMedDate not supplied

Uncoupling proteins in human heart.

Abnormal energetic activity in heart failure correlates inversely with plasma free-fatty-acid concentrations. However, the link between energetic and metabolic abnormalities is unknown. To investigate this association, we obtained blood samples from 39 patients undergoing coronary artery bypass graft surgery. Patients fasted overnight before samples were taken. When plasma free-fatty-acid concentrations were raised, cardiac mitochondrial uncoupling proteins (UCP) increased (isoform UCP2, p<0.0001; isoform UCP3, p=0.0036) and those of glucose transporter (GLUT4) protein decreased (cardiac, p=0.0001; skeletal muscle, p=0.0006). Consequently, energy deficiency in heart failure might result from increased mitochondrial UCPs (ie, less efficient ATP synthesis) and depleted GLUT4 (ie, reduced glucose uptake). New treatment to correct these energy defects would be to simultaneously lower plasma free fatty acids and provide an alternative energy source.

Adenosine Triphosphate↗