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Ravi P Mahajan
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ABSTRACT: Following the overwhelming evidence of adverse events in hospital practice, the World Health Organization (WHO)'s World Alliance for Patient Safety has launched the 'Safe Surgery Saves Lives' campaign, which has developed a surgical safety checklist aimed to improve patient safety. The implementation of this checklist has met with mixed reactions in different institutions. Many countries have still not adopted its use. In this article, a brief review is presented regarding the role of the WHO checklist, barriers to its implementation and strategies for successful adoption.
Baillière' s Best Practice and Research in Clinical Anaesthesiology 06/2011; 25(2):161-8.
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ABSTRACT: To provide recent evidence of safety in anesthesia and appraise the role of established tools of safety improvement in anesthesia practice.
The current incidence of minor events or complications during anesthesia is estimated at 18-22%, for severe complications 0.45-1.4%, and for mortality of 1: 100 000. Evidence suggests that despite such low complication rates, further improvements can still be made by addressing systemic factors which are known to set up conditions for adverse events. In particular, improvements can be made in the areas of drug errors, and inadequate or lack of communication between different clinical teams during the process of handovers. In addition, the evidence is growing which highlights the importance of established tools such as critical incident reporting, quality management using plan-do-check-act cycles, use of checklists and use of simulation in training clinical staff in the areas of nontechnical skills.
Anesthesia is one of the safest clinical specialties and remains at the top among leaders of patient safety. This review provides evidence for the areas in which further progress can be made, and usefulness of certain tools, such as critical incident reporting, checklists, plan-do-check-act cycles and simulation, can be used for continued improvements.
Current opinion in anaesthesiology 02/2011; 24(3):349-53.
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ABSTRACT: The zero flow pressure (ZFP) is the pressure at which blood flow ceases through a vascular bed. Using transcranial Doppler ultrasonography, we investigated the effects of propofol or sevoflurane on the estimated cerebral perfusion pressure (eCPP) and ZFP in the cerebral circulation. Twenty-three healthy patients undergoing nonneurosurgical procedures under general anesthesia were studied. After induction of anesthesia using propofol, the anesthesia was maintained with either propofol infusion (n = 13) or sevoflurane (n = 10). Middle cerebral artery flow velocity, noninvasive arterial blood pressure, and end-tidal carbon dioxide partial pressure were recorded awake as a baseline, and during steady-state anesthesia at normocapnia (baseline end-tidal carbon dioxide partial pressure) and hypocapnia (1 kPa below baseline). The eCPP and ZFP were calculated using an established formula. The mean arterial blood pressure decreased in both groups. The eCPP decreased significantly in the propofol group (median, from 58 to 41 mm Hg) but not in the sevoflurane group (from 60 to 62 mm Hg). Correspondingly, ZFP increased significantly in the propofol group (from 25 to 33 mm Hg) and it decreased significantly in the sevoflurane group (from 27 to 7 mm Hg). Hypocapnia did not change eCPP or ZFP in the propofol group, but it significantly decreased eCPP and increased ZFP in the sevoflurane group.
Anesthesia & Analgesia 04/2005; 100(3):835-40, table of contents. · 3.29 Impact Factor
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ABSTRACT: Zero flow pressure (ZFP) in the cerebral circulation is defined as the arterial pressure at which flow ceases. Noninvasive methods of estimating cerebral perfusion pressure (CPP) and ZFP using transcranial Doppler ultrasonography have been described. There is a paucity of normal physiological data related to changes in estimated CPP (eCPP) and ZFP induced by changes in carbon dioxide (CO(2)). We studied the effects of CO(2) on eCPP and ZFP in 17 healthy volunteers. After baseline measurements of middle cerebral artery blood-flow velocity and blood pressure, subjects voluntarily hyperventilated to decrease their end-tidal CO(2) (PE'CO(2)) by approximately 7.5 mm Hg, and then they increased their PE'CO(2) by approximately 7.5 mm Hg by breathing through a Mapleson D circuit. Blood-flow velocity and blood pressure were recorded at each stage. The eCPP and ZFP were calculated by using established formulas, and the results were analyzed with analysis of variance. With increasing PE'CO(2), eCPP increased from 50.67 mm Hg (8.33 mm Hg) (mean [SD]) to 60.87 mm Hg (9.28 mm Hg) (20% increase; P < 0.001), with a corresponding decrease in ZFP (P = 0.017); hypocapnia resulted in the opposite effects on eCPP and ZFP. These results indicate physiological changes in eCPP and ZFP that can be expected from changes in CO(2) in subjects without any neurological disorder. IMPLICATIONS: Increasing end-tidal CO(2) increases the estimated cerebral perfusion pressure and vice versa. These results are opposite to those expected from the known effects of CO(2) on intracranial pressure. Thus, we support the suggestion that, in the absence of intracranial hypertension, vascular tone remains a major determinant of effective downstream pressure and cerebral perfusion.
Anesthesia & Analgesia 04/2003; 96(3):847-51, table of contents. · 3.29 Impact Factor
