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Biomedical subjects

R I Hall

Publications and source records attributed to R I Hall.

At least 19 recordsLinked to original sources

Dynamics and post-collision interaction effects in two electron decay from the Xenon 4d hole.

Two Auger electrons, one very slow, one fast, have been detected in coincidence following near threshold 4d photoionization of the Xe atom. The distribution in the energy the two electrons share has been measured for the first time revealing the presence of post-collision interaction effects that provide unique information on the decay dynamics of the 4d hole. Analysis of the distorted line shapes indicates that the dominant process is decay of Xe+(4d(-1)) to Xe3+ through cascade emission of a zero kinetic energy Auger electron followed by a fast Auger electron. The widths of the intermediate Xe2+* states are estimated to be about 60 meV.

Journal Article↗

Observation of triplet doubly excited states in single photon excitation from ground state helium.

We have observed, for the first time, LS-forbidden triplet doubly excited states, in single photon excitation of ground state helium, below the second ionization threshold. These states are identified as (3)D(o) and (3)P(o) and their excitation is due to spin-orbit interaction that mixes them with the optically allowed (1)P(o) states. This observation is possible due to the very high efficiency in detecting metastable atoms created after the fluorescence decay of the doubly excited states, and the new capabilities of third generation synchrotron vacuum ultraviolet sources with high resolution beam lines.

Journal Article↗

Propofol vs midazolam for ICU sedation : a Canadian multicenter randomized trial.

STUDY OBJECTIVES: To determine whether sedation with propofol would lead to shorter times to tracheal extubation and ICU length of stay than sedation with midazolam. DESIGN: Multicenter, randomized, open label. SETTING: Four academic tertiary-care ICUs in Canada. PATIENTS: Critically ill patients requiring continuous sedation while receiving mechanical ventilation. INTERVENTIONS: Random allocation by predicted requirement for mechanical ventilation (short sedation stratum, < 24 h; medium sedation stratum, > or = 24 and < 72 h; and long sedation stratum, > or = 72 h) to sedation regimens utilizing propofol or midazolam. MEASUREMENTS AND RESULTS: Using an intention-to-treat analysis, patients randomized to receive propofol in the short sedation stratum (propofol, 21 patients; midazolam, 26 patients) and the long sedation stratum (propofol, 4 patients; midazolam, 10 patients) were extubated earlier (short sedation stratum: propofol, 5.6 h; midazolam, 11.9 h; long sedation stratum: propofol, 8.4 h; midazolam, 46.8 h; p < 0.05). Pooled results showed that patients treated with propofol (n = 46) were extubated earlier than those treated with midazolam (n = 53) (6.7 vs 24.7 h, respectively; p < 0.05) following discontinuation of the sedation but were not discharged from ICU earlier (94.0 vs 63.7 h, respectively; p = 0.26). Propofol-treated patients spent a larger percentage of time at the target Ramsay sedation level than midazolam-treated patients (60.2% vs 44.0%, respectively; p < 0.05). Using a treatment-received analysis, propofol sedation either did not differ from midazolam sedation in time to tracheal extubation or ICU discharge (sedation duration, < 24 h) or was associated with earlier tracheal extubation but longer time to ICU discharge (sedation duration, > or = 24 h, < 72 h, or > or = 72 h). CONCLUSIONS: The use of propofol sedation allowed for more rapid tracheal extubation than when midazolam sedation was employed. This did not result in earlier ICU discharge.

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Acute Disease↗

End-of-life care in the ICU: treatments provided when life support was or was not withdrawn.

STUDY OBJECTIVE: To compare and contrast use of technology, pharmacology, and physician variability in end-of-life care of ICU patients dying with or without active life support. DESIGN: Retrospective cohort study. SETTING: Two medical-surgical tertiary-care ICUs in a Canadian regional referral teaching hospital. PARTICIPANTS: One hundred seventy-four patients who died between July 1, 1996, and June 30, 1997. INTERVENTION: Data abstraction from medical records. RESULTS: Patients in whom life support was withheld or withdrawn (138 of 174, 79%) were older (65 +/- 16 years vs 55 +/- 18 years; p < 0.05 [mean +/- SD]). Once the decision to withdraw life support was made, death occurred in 4.3 h (2.1 to 6.5 h; mean [95% confidence interval]). Patients who had active life support treatment until death received more support measures including inotropic agents (36 of 36 vs 21 of 138; p < 0.05), dialysis (4 of 36 vs 2 of 138; p < 0.05), and mechanical ventilation at the time of death (36 of 36 vs 81 of 138; p < 0.05). Physician differences (> 10-fold) were detected for prescribed doses of morphine and sedative agents whether or not life support was withheld or withdrawn. The median cumulative dose of morphine prescribed during the final 12 h was larger (fivefold) in patients undergoing withdrawal of life support. No documented discussion of life support withdrawal was noted in one case. In the remaining patients, the 10 staff physicians were documented to be involved in 77% (range, 54 to 94%) of the end-of-life discussions. CONCLUSIONS: Differences were evident in technologic and pharmacologic support and in physician prescribing habits in patients for whom life support was or was not withheld or withdrawn. Substantial variability was noted in physician documentation of physician-family interactions surrounding the withdrawal of life support.

Age Factors↗

A prospective evaluation of empiric versus protocol-based sedation and analgesia.

STUDY OBJECTIVE: To compare empiric and protocol-based therapies of sedation and analgesia in terms of pharmacologic cost, effects on mechanical ventilation and intensive care unit (ICU) stay, and quality of sedation and analgesia. DESIGN: Prospective study. SETTING: A 24-bed medical-surgical-neurologic ICU. PATIENTS: Seventy-two patients evaluated during empiric therapy and 86 during protocol-based therapy. INTERVENTION: Assessment of data collected for 4 months before and 5 months after an evidence-based sedation and analgesia protocol was implemented. MEASUREMENTS AND MAIN RESULTS: Protocol adherence rate was 83.7%. The hourly cost (Canadian dollars) of sedation was less with protocol-based therapy ($5.68 +/- 4.27 vs $7.69 +/- 5.29, p<0.01) likely due to increased lorazepam use. Pharmacologic cost savings may be negated since sedation duration tended to be longer (122.7 +/- 142.8 vs 88.0 +/- 94.8 hrs, p<0.1) and extubation may have been delayed (61.6 +/- 97.4 vs 39.1 +/- 54.7 hrs, p=0.13) with protocol use. Duration of ICU stay after sedation was discontinued was not significantly different before and after protocol implementation. With the protocol, however, the percentage of modified Ramsay sedation scores representing discomfort decreased from 22.4 to 11% (p<0.001) and the percentage at a score of 4 increased from 17.2% to 29.6% (p<0.01). The percentage of modified visual analog measurements representing pain decreased from 9.6 to 5.9% (p<0.05) with the protocol. When data were stratified according to duration of sedation, the benefits and delayed extubation associated with protocol-based therapy were limited to patients requiring long-term sedation. CONCLUSION: Compliance with this protocol reduced drug costs and enhanced the quality of sedation and analgesia for patients requiring long-term sedation. Protocol-based therapy with lorazepam may have delayed extubation but did not delay ICU discharge.

Analgesia↗

Limited resuscitation with hypertonic saline, hypertonic sodium acetate, and lactated Ringer's solutions in a model of uncontrolled hemorrhage from a vascular injury.

BACKGROUND: Hypertonic sodium acetate-dextran solution (HAD) causes vasodilatation and buffers metabolic acidosis. In controlled hemorrhage models, HAD in small volumes increases cardiac output without increasing blood pressure, thus creating a "high flow-low pressure" state. The objective of this study was to determine whether limited resuscitation of uncontrolled hemorrhage with HAD solution improves gut perfusion as measured by intestinal mucosal tonometry. METHODS: Three groups of 10 swine were bled 25 mL/kg by means of a femoral artery catheter to produce a mean blood pressure of 30 mm Hg. A 4-mm abdominal aortic laceration was then produced by pulling out a preimplanted wire loop. Groups were then randomly assigned to be resuscitated with either lactated Ringer's solution, a hypertonic saline-dextran solution or HAD solution sufficient to maintain a mean blood pressure of 45 mm Hg for 5 hours or until death. Outcomes were measured by survival, intraperitoneal blood loss, hemodynamic monitoring, and ileal mucosal tonometry. RESULTS: HAD infusions caused transient worsening of hypotension and were associated with increased mortality (p = 0.038). Blood loss and volumes required for resuscitation were significantly increased in the lactated Ringer's solution group. HAD showed significant buffering effect against metabolic acidosis in arterial blood only, but intestinal ileal mucosal tonometry was not different among the groups. CONCLUSION: HAD did not improve gut perfusion despite buffering the systemic acidosis of shock and caused increased mortality. Limited resuscitation with any of these solutions is associated with significant mucosal acidosis.

Acid-Base Equilibrium↗

Midazolam-sufentanil vs sufentanil-enflurane for induction of anaesthesia for CABG surgery.

PURPOSE: To compare the effects of midazolam-sufentanil (Group I) and sufentanil-enflurane (Group II) anaesthesia on myocardial oxygenation and metabolism in patients with preserved ventricular function undergoing CABG surgery. METHODS: Patients randomized to Group I (n = 16) received midazolam 0.3 mg.kg-1 at induction of anaesthesia, 0.15 mg.kg-1 after tracheal intubation, followed by an infusion of 2.5-10.0 micrograms.kg-1.min-1. Supplemental sufentanil (cumulative maximum of 5 micrograms.kg-1) was given for adverse haemodynamic responses. Group II (n = 16) received 5 micrograms.kg-1 sufentanil at induction. Additional sufentanil (maximum 5 micrograms.kg-1), and enflurane (0-3% inspired concentration) were administered for adverse haemodynamic responses. Haemodynamics, myocardial oxygen consumption (MVO2), and lactate extraction were determined at the following times: I) awake (AWA), 2) after induction (IND), and 3) after tracheal intubation (ETT). RESULTS: Systemic haemodynamics and myocardial metabolism were similar at AWA. Heart rate response was attenuated and MVO2 reduced in Group I at IND (P < 0.05). Following AWA, myocardial lactate production (MLP) occurred more frequently in Group II vs Group I patients (9/16 vs 2/16) and at more individual measurement points (Group II: 10/64 vs Group I: 3/64). Myocardial lactate flux demonstrated a deleterious trend in Group II at ETT. CONCLUSIONS: Compared with sufentanil-enflurane, midazolam-sufentanil anaesthesia resulted in comparable and acceptable haemodynamics and myocardial oxygenation in CABG patients.

Analysis of Variance↗

Effect of pressure on myocardial function after 6-hour preservation with blood cardioplegia.

BACKGROUND: This study examined the return of cardiac function in pig hearts after 6 hours' preservation by continuous perfusion with blood cardioplegia at two perfusion pressures compared with preservation with crystalloid solutions. METHODS: Isolated pig hearts were randomly divided into five groups (n = 8 per group) according to the following treatments: group 1 = fresh hearts (control); group 2 = hearts arrested with Queen's cocktail cardioplegia and then immersion in 0 degrees C saline solution (QS group); group 3 = hearts arrested with (5 degrees C) and simple immersion in 0 degrees C University of Wisconsin solution (UW group); and groups 4 and 5 = hearts arrested with blood cardioplegia at 10 degrees C and then continuously perfused at a pressure of 80 cm H2O or 40 cm H2O, respectively (groups BC80 and BC40). After preservation for 6 hours, donor hearts were reperfused by a cross-circulation support pig. Thereafter, cardiac function and metabolism were examined every half hour for 2 hours. A three-way mixed general linear model was used to analyze data with repeated measures. Bonferroni test was used to determine differences (p < or = 0.05) between groups. RESULTS: Only 4 hearts recovered electric activity in the BC80 group (p < or = 0.05 versus other groups). There was poor recovery of left ventricular work in the BC80 group compared with the other groups (p < 0.001). Left ventricular work in the QS and UW groups was also lower than in the control and BC40 groups. Left ventricular work in the BC40 group fully recovered. Maximum elastance did not differ between groups. Compliance was reduced in the QS, BC80, and BC40 groups versus controls after preservation (p < 0.006). Coronary flow decreased and coronary vascular resistance increased in the BC80 group versus the other groups (p < or = 0.001). Coronary flow in the QS, UW, and BC40 groups was lower than in the control group (p < 0.001). The magnitude of lactate release was much higher in the BC80 group than in the other groups (p < or = 0.001). CONCLUSIONS: Continuous perfusion with 10 degrees C blood cardioplegia at 40 cm H2O pressure for 6 hours provided adequate preservation of systolic function in this model. University of Wisconsin solution provided the best protection of diastolic function.

Adenosine↗

Factors influencing MAC reduction after cardiopulmonary bypass in dogs.

BACKGROUND: Anaesthetic requirements may be reduced following surgery employing cardiopulmonary bypass (CPB). This study, in dogs, determined the role of a) volatile agents (enflurane [E] vs isoflurane [I]), b) oxygenator (bubble [B] vs membrane [M]), and c) presence [FL] vs absence [NoFL] of an in-line arterial filter in the bypass circuit in altering anaesthetic requirements following CPB. METHODS: Male mongrel dogs were anaesthetized with either enflurane (n = 24) or isoflurane (n = 24). They were randomly assigned to one of eight groups (n = 6 per group); Group 1 (E/B/FL), Group 2 (E/M/FL), Group 3 (E/M/NoFL), Group 4 (E/B/NoFL), Group 5 (I/M/FL), Group 6 (I/B/FL), Group 7 (I/M/NoFL) or Group 8 (I/B/NoFL). MAC was determined using the tail-clamp method at hourly intervals, twice before and three times after a one hour normothermic perfusion using aortoatrial cannulation and CPB. RESULTS: Prior to CPB, MAC was reproducible (enflurane: MAC1 2.17 +/- 0.29 vs MAC2 2.14 +/- 0.28%; isoflurane: MAC1 1.42 +/- 0.31 vs MAC2 1.41 +/- 0.33%) and differed among groups only for the volatile agent employed. Following CPB, MAC was reduced in all groups (P < 0.05 vs pre-CPB measurements) except Group 1 (E/B/FL). The degree of MAC reduction in other groups ranged from 39-64% and was not different based on type of agent employed, use of a membrane or bubble oxygenator, or presence or absence of an in-line arterial filter. CONCLUSION: In dogs, MAC reduction following CPB was variable, not related to type of volatile agent employed, use of a membrane or bubble oxygenator, or presence or absence of an in-line arterial filter. The explanation for reductions in anaesthetic requirements following CPB in this model remains speculative.

Anesthetics↗

Light versus heavy sedation after cardiac surgery: myocardial ischemia and the stress response. Maritime Heart Centre and Dalhousie University.

UNLABELLED: The influence of light versus heavy sedation after coronary artery bypass graft (CABG) surgery on the development of postoperative myocardial ischemia has not been described. After uncomplicated CABG surgery, 50 patients were randomly assigned to receive LOW (n = 24; target Ramsay Sedation Score [RSS] = 2) or HIGH (n = 26; target RSS = 4) sedation with propofol. Analgesia was provided to maintain a visual analog scale (VAS) pain score <7. Myocardial ischemia was identified perioperatively using continuous 3-lead Holter monitoring. By measuring creatine kinase (CK) MB levels preoperatively, at entry to the intensive care unit (ICU), and every 12 h for 48 h; and by obtaining serial 12-lead electrocardiograms (ECG) (preoperatively; 2, 4, 12, 24, and 48 h after ICU admission, 8:00 AM the morning after surgery; and 5 min pre- and postextubation), myocardial infarction was identified. Endocrine stress response was assessed by measuring serum cortisol levels preoperatively, on admission to the ICU, and 24 h postoperatively. In a subset of patients (LOW n = 10, HIGH n = 11), plasma and urinary catecholamine levels were also measured. There were no between-group differences in demographics, operative course, hemodynamic variables, or cortisol levels while in the ICU. The VAS pain score and target RSS were achieved and sustained, and they differed between groups. There were three myocardial infarctions in each group by CKMB criteria alone. No ECG-identifiable myocardial infarction occurred. The ST segment versus time curve (LOW 187 +/- 295 versus HIGH 1071 +/- 2137 mm/min) differed between groups. Urinary and plasma catecholamine levels were similar between groups over the observation period. We conclude that the use of a reduced sedation regimen in combination with adequate analgesia did not result in an increased endocrine stress response or risk of myocardial ischemia. IMPLICATIONS: This randomized study of patients after coronary artery bypass surgery examined whether light (versus heavy) sedation with propofol in the intensive care unit was associated with an increased degree of myocardial ischemia. Using techniques to detect myocardial ischemia, including Holter monitoring, electrocardiogram, and myocardial enzyme measurements, no differences were found. We conclude that light sedation does not increase the endocrine stress response or the risk of myocardial infarction.

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