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Historically, surgical instruments were designed by men for male surgeons. Although instrumentation has changed with the changing paradigms of surgery, it has failed to adapt to the changing surgical workforce. Almost 30% of surgeons are female and nearly 90% of surveyed female surgeons report poor instrument design and associated musculoskeletal injuries from use. Understanding the current state of handheld surgical instrument design, published literature was reviewed, surgical instrument collections were contacted, and the U.S. Patent and Trademark databases were queried to identify public patents and pre-granted applications of female inventors of handheld surgical instruments. Twenty-five female inventors were identified from published literature and 1551 unique females hold patents. This number pales when the denominator of male inventors is considered. Hence, to address the female surgeon’s lack of instrumentation and design, there is a critical need for participatory ergonomics whereby both the female surgeon and engineer collaborate on design.

The high number of patients infected with the SARS-CoV-2 virus requiring care for ARDS puts sedation in the critical care unit (CCU) to the edge. Depth of sedation has evolved over the last 40 years (no-sedation, deep sedation, daily emergence, minimal sedation, etc.). Most guidelines now recommend determining the depth of sedation and minimizing the use of benzodiazepines and opioids. The broader use of alpha-2 adrenergic agonists (‘alpha-2 agonists’) led to sedation regimens beginning at admission to the CCU that contrast with hypnotics+opioids (“conventional“ sedation), with major consequences for cognition, ventilation and circulatory performance. The same doses of alpha-2 agonists used for ‘cooperative’ sedation (ataraxia, analgognosia) elicit no respiratory depression but modify the autonomic nervous system (cardiac parasympathetic activation, attenuation of excessive cardiac and vasomotor sympathetic activity). Alpha-2 agonists should be selected only in patients who benefit from their effects (‘personalized’ indications, as opposed to a ‘one size fits all’ approach). Then, titration to effect is required, especially in the setting of systemic hypotension and/or hypovolemia. Since no general guidelines exist for the use of alpha-2 agonists for CCU sedation, our clinical experience is summarized for the benefit of physicians in clinical situations in which a recommendation might never exist (refractory delirium tremens; unstable, hypovolemic, hypotensive patients, etc.). Because the physiology of alpha-2 receptors and the pharmacology of alpha-2 agonists lead to personalized indications, some details are offered. Since interactions between conventional sedatives and alpha-2 agonists have received little attention, these interactions are addressed. Within the existing guidelines for CCU sedation, this article could facilitate the use of alpha-2 agonists as effective and safe sedation while awaiting large, multicentre trials and more evidence-based medicine.

The difficulty of defining the three so-called components of « an-esthesia » is emphasized: hypnosis, absence of movement, and adequacy of anti-nociception (intraoperative « analgesia »). Data obtained from anesthetized animals or humans delineate the activation of cardiac and vasomotor sympathetic reflex (somato-sympathetic reflex) and the cardiac parasympathetic deactivation observed following somatic stimuli. Sympathetic activation and parasympathetic deactivation are used as monitors to address the adequacy of intraoperative anti-nociception. Finally, intraoperative nociception through the administration of nonopioid analgesics vs. opioid analgesics is considered to achieve minimal postoperative side effects.

ABSTRACTDuring severe septic shock and/or severe acute respiratory distress syndrome (ARDS) patients present with a limited cardio-ventilatory reserve (low cardiac output and blood pressure, low mixed venous saturation, increased lactate, low PaO2/FiO2 ratio, etc.), especially when elderly patients or co-morbidities are considered. Rescue therapies (low dose steroids, adding vasopressin to noradrenaline, proning, almitrine, NO, extracorporeal membrane oxygenation, etc.) are complex. Fever, above 38.5–39.5°C, increases both the ventilatory (high respiratory drive: large tidal volume, high respiratory rate) and the metabolic (increased O2 consumption) demands, further limiting the cardio-ventilatory reserve. Some data (case reports, uncontrolled trial, small randomized prospective trials) suggest that control of elevated body temperature (“fever control”) leading to normothermia (35.5–37°C) will lower both the ventilatory and metabolic demands: fever control should simplify critical care management when limited cardio-ventilatory reserve is at stake. Usually fever control is generated by a combination of general anesthesia (“analgo-sedation”, light total intravenous anesthesia), antipyretics and cooling. However general anesthesia suppresses spontaneous ventilation, making the management more complex. At variance, alpha-2 agonists (clonidine, dexmedetomidine) administered immediately following tracheal intubation and controlled mandatory ventilation, with prior optimization of volemia and atrio-ventricular conduction, will reduce metabolic demand and facilitate normothermia. Furthermore, after a rigorous control of systemic acidosis, alpha-2 agonists will allow for accelerated emergence without delirium, early spontaneous ventilation, improved cardiac output and micro-circulation, lowered vasopressor requirements and inflammation. Rigorous prospective randomized trials are needed in subsets of patients with a high fever and spiraling toward refractory septic shock and/or presenting with severe ARDS.

One way to identify central cardiovascular neurons is to consider their barosensitivity, for example by plotting changes in their single unit activity as a function of evoked changes in blood pressure. To simplify the genesis of such pressure-activity relationships, a coronary angioplasty catheter was threaded into the aorta of anaesthetized rats and the balloon inflated to raise the blood pressure mechanically. Here, such a procedure is exemplified for cardiac vagal motoneurons in the medulla oblongata in eight rats. This simplification bypasses potentially problematic surgery and minimizes deterioration of the animal. Experimental Physiology (2002) 87.5, 535-538.

One way to identify central cardiovascular neurons is to consider their barosensitivity, for example by plotting changes in their single unit activity as a function of evoked changes in blood pressure. To simplify the genesis of such pressure‐activity relationships, a coronary angioplasty catheter was threaded into the aorta of anaesthetized rats and the balloon inflated to raise the blood pressure mechanically. Here, such a procedure is exemplified for cardiac vagal motoneurons in the medulla oblongata in eight rats. This simplification bypasses potentially problematic surgery and minimizes deterioration of the animal.

Experimentally, α2-agonists keep intact the reactivity of the circulatory system to hypotension or hypovolaemia. These findings have been reproduced in humans outside the anaesthesia/critical care setting. Within the anaesthesia/critical care setting, no studies directly tackle the problem of circulatory reactivity to hypotension. Poor circulatory tolerance (hypotension, bradycardia and low cardiac output) to systemic α2-agonists has been reported in the anaesthetic setting. In contrast, however, most reports in the literature suggest good tolerance. This discrepancy may be a function of the intravascular volume status, the dosage of the anaesthetic/sedative agents co-administered or the specific opiate used. The opinion of the authors is that (a) the administration of α2-agonists should be restricted to hypertensive/coronary patients or patients presenting to or recovering from minor or major surgery in whom a high benefit-to-risk ratio is expected, (b) appropriate volume loading before the induction of anaesthesia or intra-hospital transport should be considered, and (c) a reduction in anaesthetic/sedative and vasopressor requirements should be considered. Key studies are lacking.

1. Using in vivo voltammetry, this study relates catecholamine metabolism within the rat rostral ventrolateral medulla to the level of mean arterial pressure (MAP) under halothane anaesthesia. 2. A vasopressor region was circumscribed with electrical stimulations in an area located 1000‐1700 microns rostral to the obex. A catechol signal was then ascertained within this area. The recording site was surrounded with phenyl‐N‐methyl‐ethanolamine transferase immuno‐positive cell bodies. 3. Three levels of decrease of arterial pressure were induced with nitroprusside infusion: ‐15, ‐35 and ‐55 mmHg (n = 5 in each group) from baseline for 30 min. This led to increases in the catechol signal which were inversely related to the degree of hypotension (P < 10(‐4) vs. saline for the 35 and 55 mmHg groups, P < 0.05 for the 35 mmHg group as compared to the 15 and 55 mmHg groups following recovery from hypotension). 4. Following sino‐aortic deafferentation, nitroprusside‐induced hypotension (‐35 mmHg) did not lead to any change in the catechol signal in the rostral ventrolateral medulla (n = 5). Furthermore, controlled hypotension induced in intact rats did not evoke any change in the catechol signal recorded in a dopaminergic area of the midbrain, the ventral tegmental area (A10 area; n = 5). 5. An infusion of phenylephrine increased MAP by 35 mmHg from a baseline pressure of 105 mmHg for 30 min and evoked a non‐significant decrease in the catechol signal (n = 5). In another group of rats a lower baseline pressure (80 mmHg) was stabilized (n = 5) with a higher concentration of halothane. An identical increment in pressure was then produced by a phenylephrine infusion and led to a significant reduction in the catechol signal (P < 0.05 vs. saline under similar conditions; n = 5). 6. The new findings of this study are that the level of activity of the metabolism of catecholamine in the rostral ventrolateral medulla (i) is continuously related to the level of arterial pressure, (ii) functions close to its resting level under baseline conditions and is primarily engaged during hypotension and (iii) is baroreflex linked. 7. Given the lack of direct evidence for a link between unit activity and catechol metabolism, these changes in catechol activity, recorded continuously in vivo next to adrenergic cell bodies, may represent the biochemical‐specific counterpart of changes in the level of electrical unitary activity of presumed adrenergic cardiovascular medullospinal sympathoexcitatory neurons. Therefore, it provides evidence that adrenaline‐synthesizing neurons in the rostral ventrolateral medulla respond to baroreceptor inputs.

Scores on the Mooney Problem Check List, a 288-item, self-administered, listing of common personal problems, for 36 borderline personality disorder inpatients and other inpatients with a diagnosis of other character disorders without borderline features were compared. Borderline patients endorsed 30% of the listing (other personality disorders 19%) and also shared more of the same problems.

Abstract:  To test in a catechol-specific and dynamic manner for the existence of a powerful long-lasting inhibition arising from barosensitive afferents that depresses the activity of adrenergic neurons in the rostral ventrolateral medulla (RVLM), in vivo voltammetry was used before and after acute sino-aortic deafferentation. Rats were anaesthetized with pentobarbital or halothane and ventilated with a mixture of air and oxygen. Snares were inserted around the vagus, the glossopharyngeal and the superior laryngeal nerves. After placing the animal prone in the stereotaxic frame and stabilization at a high mean arterial pressure (MAP ≈ 120 mmHg), the snares were rapidly closed to produce complete barodeafferentation, assessed by loss of heart rate responses and changes in renal nerve sympathetic activity in response to vasoactive agents. Recording of a catechol signal was maintained in the RVLM during deafferentation. Under pentobarbital-induced anaesthesia (n = 5), deafferentation did not lead to a significant change in the catechol signal within the deafferented group. Under halothane-induced anaesthesia and phenylephrine-induced high baseline pressure (n = 5), no changes in the catechol signal were observed upon deafferentation (not significant vs sham animals: n = 5). This failure to demonstrate a major increase in catechol activity upon deafferentation does not fit with the hypothesis that a powerful tonic baroreflex-mediated inhibition depresses the activity of adrenergic RVLM barosensitive bulbospinal neurons, even when the baseline MAP is high. Rather, these data are compatible with weak or no inhibition of catechol activity by the baroreceptors and a nonessential role of adrenergic neurons within the baroreceptor reflex arc itself: the adrenergic neurons may not be in series within this arc but in parallel with the arc. This interpretation is in keeping with newer schemas of autonomic core circuitry that are devoid of adrenergic neurons.

The rostral ventrolateral medulla (RVLM) controls the vascular system. It may contribute to postoperative hypertension observed upon emergence from anesthesia. This structure contains adrenergic cardiovascular neurons. Therefore, one question was addressed: does a change in RVLM catechol activity occur upon emergence from anesthesia? Halothane‐anesthetized, paralyzed rats had their ventilatory, circulatory, and acid‐base stability controlled. All pressure points and incisions were infiltrated with local anesthetic. With in vivo electrochemistry, a catechol signal was recorded in the RVLM in the following circumstances: (1) under stable halothane anesthesia for 120 minutes (halothane group), (2) during 120 minutes after halothane discontinuation (saline‐emergence group), (3) during 60 minutes after halothane discontinuation followed by 60 minutes after halothane readministration (readministration group), (4) emergence in rats treated with atenolol and nitroprusside to hold blood pressure as close as possible to baseline, (5) emergence after morphine 1 mg.kg−1i.v., (6) emergence after decerebration, and (7) emergence upon recording in the mid‐brain dopaminergic A10 area. Stable halothane anesthesia (n = 6) led to no change in mean arterial pressure (MAP), heart rate (HR), and catechol signal (CAOC). During emergence from anesthesia (n = 6), MAP, HR, and catechol signal increased and did not return to baseline. By contrast, a return of MAP, HR, and catechol signal to baseline was observed upon readministration of halothane (n = 6). Whereas blood pressure and heart rate were maintained as closely as possible to baseline, a large catechol activation (n = 5) was observed upon emergence from anesthesia. A catechol activation from a lowered baseline was observed upon emergence following morphine administration (n = 5). A minor circulatory activation without RVLM catechol activation was observed upon emergence following decerebration (n = 5). Recordings in the A10 area revealed no increase in the catechol signal following emergence (n = 5). Adrenergic RVLM neurons appear to be responsive upon emergence from anesthesia, possibly being activated by suprapontine afferents impinging on the RVLM. Synapse 30:130–139, 1998.© 1998 Wiley‐Liss, Inc.

The rostral ventrolateral medulla (RVLM) controls the vascular system. It may contribute to postoperative hypertension observed upon emergence from anesthesia. This structure contains adrenergic cardiovascular neurons. Therefore, one question was addressed: does a change in RVLM catechol activity occur upon emergence from anesthesia? Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and acid-base stability controlled. All pressure points and incisions were infiltrated with local anesthetic. With in vivo electrochemistry, a catechol signal was recorded in the RVLM in the following circumstances: (1) under stable halothane anesthesia for 120 minutes (halothane group), (2) during 120 minutes after halothane discontinuation (saline-emergence group), (3) during 60 minutes after halothane discontinuation followed by 60 minutes after halothane readministration (readministration group), (4) emergence in rats treated with atenolol and nitroprusside to hold blood pressure as close as possible to baseline, (5) emergence after morphine 1 mg.kg⁻¹ i.v., (6) emergence after decerebration, and (7) emergence upon recording in the mid-brain dopaminergic A10 area. Stable halothane anesthesia (n = 6) led to no change in mean arterial pressure (MAP), heart rate (HR), and catechol signal (CAOC). During emergence from anesthesia (n = 6), MAP, HR, and catechol signal increased and did not return to baseline. By contrast, a return of MAP, HR, and catechol signal to baseline was observed upon readministration of halothane (n = 6). Whereas blood pressure and heart rate were maintained as closely as possible to baseline, a large catechol activation (n = 5) was observed upon emergence from anesthesia. A catechol activation from a lowered baseline was observed upon emergence following morphine administration (n = 5). A minor circulatory activation without RVLM catechol activation was observed upon emergence following decerebration (n = 5). Recordings in the A10 area revealed no increase in the catechol signal following emergence (n = 5). Adrenergic RVLM neurons appear to be responsive upon emergence from anesthesia, possibly being activated by suprapontine afferents impinging on the RVLM. Synapse 30:130–139, 1998. © 1998 Wiley-Liss, Inc.

This study attempted to distinguish the borderline personality disorder (BPD) from other personality disorders (OPD) on the basis of the Lachar and Wrobel critical item list. Seventy-five male psychiatric inpatients with diagnoses fitting DSM-III criteria for BPD and OPD and ranging in age from 24 to 47 years completed the MMPI. Lachar's critical item set, composed of 111 items taken from the MMPI, was then selected from each of the 75 subjects' response items. BPD and OPD patients significantly differed on only the Lachar Substance Abuse subscale. Implications of this study are discussed with regard to the concept that personality structure involves a continuum of psychopathology. The Lachar critical item list provided support for drug abuse as part of the diagnostic criteria for BPD and displayed promise for identifying areas of psychopathology on which treatment may be focused.

The symbol for symbiosis, used within transactional analysis to convey the concept of an unnatural social interdependency between parent and child, is extended into a chain in order to symbolize a phenomenon observed within the chain of command of organizations involved in rendering noncompetitive routine services. The symbiotic chain symbol represents the extension of social interdependency downward through one to several levels of supervision. The chain's effect is to isolate top management from the creative and innovative ideas of autonomous individuals at the journeyman level. The chain's impact on promotion creates a paucity of leadership-in-depth in the workplace by reducing the probability of promotion of autonomous individuals.

Describes built in cultural need to help others and describes how this trait may be adversely exploited by others.

After completion of abdominal aortic graft, 29 patients received an i.v. infusion of placebo (n = 16) or clonidine 7 μg kg−1 (n = 13) over 120 min in a double-blind study. Cardiovascular variables were measured and plasma samples obtained up to 5 h after arrival in the recovery room, for assay of noradrenaline, adrenaline, vasopressin and renin concentrations. Noradrenaline, adrenaline and vasopressin concentrations decreased in the clonidine group throughout recovery (P < 0.001, 0.05 and 0.05, respectively, vs placebo). Heart rate was less in the clonidine group (P < 0.01). There was no significant difference in mean arterial pressure between groups. Stroke volume was larger (P < 0.01) and there were fewer episodes of hypertension (P < 0.05) and tachycardia in the clonidine group. In addition, a reduction in the number of circulatory interventions (P < 0.05) and episodes of shivering was noted in the clonidine group. Mean (SD) postoperative volume requirements were larger in the clonidine group (total postoperative input: clonidine 1462 (604) ml; placebo 1064 (348) ml (P < 0.05)). These data are consistent with the observation that clonidine modifies endocrine and circulatory status after major surgery.