High-inspired oxygen concentration further impairs opioid-induced respiratory depression.

BACKGROUND: Hyperoxaemia depresses the output of peripheral and central chemoreceptors. Patients treated with opioids often receive supplemental oxygen to avert possible decreases in oxygen saturation (Sp(O2)).We examined the effect of a single dose of remifentanil in healthy volunteers inhaling room air vs air enriched with 50% oxygen. METHODS: Twenty healthy volunteers received i.v. 50 mg remifentanil (infused over 60 s) at anormoxic (N) or hyperoxic (FI(O2) 0.5, H) background on separate occasions. Minute ventilation (Vi), respiratory rate (RR), end-tidal PC(O2), and Sp(O2) were collected on a breath to-breath basis. The occurrence of apnoea was recorded. RESULTS: During normoxia, remifentanil decreased Vi from 7.4 (1.3) [mean (SD)] to 2.2 (1.2) litre min 21 (P,0.01), and during hyperoxia from 7.9 (1.0) to 1.2 (1.2) litre min 21 (P,0.01; H vs N: P,0.001). RR decreased from 13.1 (2.9) to 6.1 (2.8) bpm during N (P,0.01) and from 13.2 (3.0) to 3.6 (4.0) bpm during H (P,0.01; H vs N: P,0.01). During normoxia, Sp(O2) decreased from 98.4 (1.5) to 88.6 (6.7)% (P,0.01), while during hyperoxia, Sp(O2) changed from 99.7 (0.7) to 98.7 (1.0)% (P,0.001). Apnoea developed in two subjects during normoxia and 10 during hyperoxia. CONCLUSIONS: Respiratory depression from remifentanil is more pronounced in hyperoxia than normoxia as determined from minute ventilation, end-tidal PC(O2), and RR. During hyperoxia, respiratory depression may be masked when measuring Sp(O2) as pulse oximetry remains in normal values during the first minutes of respiratory depression.

Confirming the drugs administered during anaesthesia: a feasibility study in the pilot National Health Service sites, UK.

BACKGROUND: To help prevent drug errors, it is recommended that drugs should be confirmed/checked with a second person before administration. We aimed to assess the feasibility of introducing second-person or electronic bar-code confirmation of drugs, administered during anaesthesia, in the National Health Service (NHS) settings in the UK. METHODS: Seven NHS sites took part in a pilot study over a 3 month period. Five used a second-person and two used bar-code electronic confirmation of drugs given during anaesthesia. A total of 36 consultant anaesthetists and three trainees, 15 operating department practitioners (ODPs), and seven anaesthetic nurses participated. A group of anaesthetists, ODPs, and nurse practitioners (n=11) from different NHS sites independently observed both methodologies. In addition, each site was visited and observed by one of the study investigators. At the end of the study period, four focus groups (two with participants from pilot sites and two with observers) were held. The discussions were taped, transcribed, and qualitatively analysed. Data were triangulated using observer's notes and investigator's reflective diaries, and processed using line-by-line coding. The codes were then synthesized into themes. RESULTS: Both methods were perceived to contribute to the prevention of drug errors. For the two-person confirmation to be carried out correctly, there should be no distraction or time pressure. The main limitation to the feasibility was that the continuous presence of the second person was not always possible. The process also met with resistance from the staff at some pilot sites. Electronic confirmation was always feasible, as it did not require the presence of a second person. It was found to be intuitive to the anaesthetist's current working practice. However, there were some practical issues related to introduction of new technology and an initial learning curve. CONCLUSIONS: The introduction of two-person confirmation to the NHS would have a significant impact on the existing working practices. Issues related to resources and a cultural change will need to be addressed. Electronic confirmation was more feasible, but the technological aspects of its integration into the operating theatre environment, and learning, will require further attention.

Critical incident reporting and learning.

The success of incident reporting in improving safety, although obvious in aviation and other high-risk industries, is yet to be seen in health-care systems. An incident reporting system which would improve patient safety would allow front-end clinicians to have easy access for reporting an incident with an understanding that their report will be handled in a non-punitive manner, and that it will lead to enhanced learning regarding the causation of the incident and systemic changes which will prevent it from recurring. At present, significant problems remain with local and national incident reporting systems. These include fear of punitive action, poor safety culture in an organization, lack of understanding among clinicians about what should be reported, lack of awareness of how the reported incidents will be analysed, and how will the reports ultimately lead to changes which will improve patient safety. In particular, lack of systematic analysis of the reports and feedback directly to the clinicians are seen as major barriers to clinical engagement. In this review, robust systematic methodology of analysing incidents is discussed. This methodology is based on human factors model, and the learning paradigm which emphasizes significant shift from traditional judicial approach to understanding how 'latent errors' may play a role in a chain of events which can set up an 'active error' to occur. Feedback directly to the clinicians is extremely important for keeping them 'in the loop' for their continued engagement, and it should target different levels of analyses. In addition to high-level information on the types of incidents, the feedback should incorporate results of the analyses of active and latent factors. Finally, it should inform what actions, and at what level/stage, have been taken in response to the reported incidents. For this, local and national systems will be required to work in close cooperation, so that the lessons can be learnt and actions taken within an organization, and across organizations. In the UK, a recently introduced speciality-specific incident reporting system for anaesthesia aims to incorporate the elements of successful reporting system, as presented in this review, to achieve enhanced clinical engagement and improved patient safety.

Transient hyperaemic response to assess skin vascular reactivity: effects of heat and iontophoresed norepinephrine.

BACKGROUND: Forearm skin vascular reactivity may be assessed using a transient hyperaemic response (THR) after 20 s of brachial artery compression. THR has been manipulated by iontophoresis of vasodilators, but not vasoconstrictors, possibly because of low baseline blood flow. The effects of vasoconstrictors on vascular reactivity of pre-dilated blood vessels are unknown. We have investigated this using locally applied heat to vasodilate the skin microcirculation before iontophoresis of norepinephrine. METHODS: Active and control laser Doppler probes measured forearm skin blood flow-flux. Three THR tests were performed before and after heating skin for 5 min, and then after iontophoresis of norepinephrine 0.1%. Iontophoresis was pulsed using 45 s periods of 75 microA and 0 current over 10 min. Three temperatures were used: unheated skin, skin at 35 degrees C, and skin at 42 degrees C. Baseline flow-flux was measured for 60 s before each set of THR tests. THR ratio (THRR) was calculated by comparing baseline flow-flux immediately before arterial compression (F1) with the maximum after release (F2): THRR=F2/F1. The average values of each group of THRR results, and baseline data, were compared using the Kruskal-Wallis test. RESULTS: Iontophoresis of norepinephrine caused significant decreases in flow-flux (P<0.005). Unheated skin and skin heated to 35 degrees C showed significant decreases in THRR after norepinephrine. THRR was abolished by heating to 42 degrees C and partially restored by iontophoresis of norepinephrine. CONCLUSIONS: Iontophoresed norepinephrine causes vasoconstriction, and it partially restores vascular reactivity in the heat-induced vasodilated skin. This may be of benefit when norepinephrine is used in clinical situations.

Validation and application of a high-fidelity, computational model of acute respiratory distress syndrome to the examination of the indices of oxygenation at constant lung-state.

BACKGROUND: Calculated venous admixture (Qs/Qt) is considered the best index of oxygenation; surrogates have been developed (Pa(O(2))/Fi(O(2)), respiratory index, and arterioalveolar PO(2) difference), but these vary with Fi(O(2)), falsely indicating a change in lung-state. Using a novel model, we aimed to quantify the behaviour of the indices of oxygenation listed above during physiological and treatment factor variation. The study is the first step in developing an accurate and non-invasive tool to quantify oxygenation defects. METHODS: We present the static and dynamic validation of a novel computational model of gas exchange in acute respiratory distress syndrome (ARDS) based upon the Nottingham Physiology Simulator. Arterial gas tension predictions were compared with data derived from ARDS patients. The subsequent study examined the indices' susceptibility to variation induced by independent changes in Fi(O(2)) (0.3-1.0), haemoglobin concentration (Hb: 6-14 g dl(-1)), oxygen consumption (VO(2): 250-350 ml min(-1)), and Pa(CO(2)) (4-8 kPa). RESULTS: Static validation produced a mean error of -0.3%, a 10-fold improvement over previous models. Dynamic validation produced a mean prediction error of -0.05 kPa for Pa(O(2)) and 0.09 kPa for Pa(CO(2)). Every parameter, especially Fi(O(2)), induced variation in all indices. The least Fi(O(2))-dependent index was Qs/Qt (variation: 5.1%). In contrast, Pa(O(2))/Fi(O(2)) varied by 77% through the range of Fi(O(2)). CONCLUSIONS: We have improved simulation of gas exchange in ARDS by using a sophisticated respiratory model. Using the validated model, we have demonstrated that the current indices of oxygenation vary with alteration in Hb, Pa(CO(2)), and VO(2) in addition to their previously well-documented dependence on Fi(O(2)).

Effects of norepinephrine and glyceryl trinitrate on cerebral haemodynamics: transcranial Doppler study in healthy volunteers.

BACKGROUND: The effects of vasoactive substances on cerebral haemodynamics are not fully known. We studied the effects of norepinephrine and glyceryl trinitrate (GTN) on cerebral haemodynamics in healthy volunteers. METHODS: The effects of norepinephrine (n=10) and GTN (n=10) on the middle cerebral artery flow velocity (MCAFV), cerebral autoregulation, reactivity to carbon dioxide, and estimated cerebral perfusion pressure (eCPP) were studied using transcranial Doppler ultrasound. Established methods were used for calculating zero flow pressure (ZFP). Measurements were made at baseline, and after i.v. infusion of the study drug to the endpoints of 25% increase in mean arterial pressure (MAP) for norepinephrine (0.02-0.1 microg kg(-1) min(-1)), or 15% decrease in MAP for GTN (0.5-2.5 microg kg(-1) min(-1)). RESULTS: The MCAFV remained unchanged with norepinephrine, but decreased slightly with GTN {from [median (inter-quartile range)] 53 (38, 62) to 48 (33, 52) cm s(-1)}. Cerebrovascular reactivity did not change significantly with either drug. The eCPP did not change significantly with norepinephrine, but increased significantly with GTN [from 49 (32, 54) to 62 (47, 79) mm Hg]. ZFP increased with norepinephrine [from 39 (28, 48) to 56 (46, 62) mm Hg] and decreased with GTN [from 35 (30, 49) to 12 (-7, 20) mm Hg]. CONCLUSIONS: Norepinephrine, despite increasing arterial pressure, did not increase the eCPP. The eCPP increased significantly with GTN, despite decreased MAP. Cerebral vascular tone is an important determinant of CPP during pharmacologically induced changes in arterial pressure.