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1.
J Anaesthesiol Clin Pharmacol ; 35(3): 326-334, 2019.
Article in English | MEDLINE | ID: mdl-31543580

ABSTRACT

BACKGROUND AND AIMS: High-quality training in advanced airway skills is imperative to ensure safe anesthetic care and develop future airway specialists. Modern airway management skills are continually evolving in response to advancing technology and developing research. Therefore, it is of concern that training provisions and trainee competencies remain current and effective. MATERIAL AND METHODS: A survey questionnaire based on the airway competencies described in the Royal College of Anaesthetists' curriculum and Difficult Airway Society guidelines was posted to all United Kingdom (UK) National Health Service hospitals to be completed by the most senior anesthetic trainee (ST 5-7, resident). RESULTS: A total of 149 responses were analyzed from 237 hospitals with eligible anesthetic trainees (response rate 63%), including 53 (36%) and 39 (26%) respondents who had completed higher and advanced level airway training respectively. Although clinical experience with videolaryngoscopy was satisfactory, poor confidence and familiarity was identified with awake fiberoptic intubation, high frequency jet ventilation, at risk extubation techniques, and airway ultrasound assessment. Only 26 (17%) respondents had access to an airway skills room or had regular airway emergency training with multidisciplinary theater team participation. Reported barriers to training included lack of training lists, dedicated teaching time, experienced trainers, and availability of equipment. CONCLUSIONS: This national survey identified numerous deficiencies in airway competencies and training amongst senior anesthetic trainees (residents) in the UK. Restructuring of the airway training program and improvements in access to training facilities are essential to ensure effective airway training and the capability to produce future airway specialists.

2.
Cardiovasc Res ; 114(10): 1313-1323, 2018 08 01.
Article in English | MEDLINE | ID: mdl-29659727

ABSTRACT

Aims: Heart failure (HF) is a pro-thrombotic state. Both platelet and vascular responses to nitric oxide (NO) donors are impaired in HF patients with reduced ejection fraction (HFrEF) compared with healthy volunteers (HVs) due to scavenging of NO, and possibly also reduced activity of the principal NO sensor, soluble guanylate cyclase (sGC), limiting the therapeutic potential of NO donors as anti-aggregatory agents. Previous studies have shown that nitrite inhibits platelet activation presumptively after its reduction to NO, but the mechanism(s) involved remain poorly characterized. Our aim was to compare the effects of nitrite on platelet function in HV vs. HF patients with preserved ejection fraction (HFpEF) and chronic atrial fibrillation (HFpEF-AF), vs. patients with chronic AF without HF, and to assess whether these effects occur independent of the interaction with other formed elements of blood. Methods and results: Platelet responses to nitrite and the NO donor sodium nitroprusside (SNP) were compared in age-matched HV controls (n = 12), HFpEF-AF patients (n = 29), and chronic AF patients (n = 8). Anti-aggregatory effects of nitrite in the presence of NO scavengers/sGC inhibitor were determined and vasodilator-stimulated phosphoprotein (VASP) phosphorylation was assessed using western blotting. In HV and chronic AF, both nitrite and SNP inhibited platelet aggregation in a concentration-dependent manner. Inhibition of platelet aggregation by the NO donor SNP was impaired in HFpEF-AF patients compared with healthy and chronic AF individuals, but there was no impairment of the anti-aggregatory effects of nitrite. Nitrite circumvented platelet NO resistance independently of other blood cells by directly activating sGC and phosphorylating VASP. Conclusion: We here show for the first time that HFpEF-AF (but not chronic AF without HF) is associated with marked impairment of platelet NO responses due to sGC dysfunction and nitrite circumvents the 'platelet NO resistance' phenomenon in human HFpEF, at least partly, by acting as a direct sGC activator independent of NO.


Subject(s)
Atrial Fibrillation/blood , Blood Platelets/drug effects , Heart Failure/blood , Nitric Oxide Donors/pharmacology , Nitric Oxide/blood , Nitroprusside/pharmacology , Sodium Nitrite/pharmacology , Stroke Volume , Ventricular Function, Left , Aged , Aged, 80 and over , Atrial Fibrillation/diagnosis , Atrial Fibrillation/physiopathology , Blood Platelets/metabolism , Case-Control Studies , Cell Adhesion Molecules/blood , Chronic Disease , Drug Resistance/drug effects , Female , Heart Failure/diagnosis , Heart Failure/physiopathology , Humans , Male , Microfilament Proteins/blood , Nitric Oxide Donors/metabolism , Nitroprusside/metabolism , Phosphoproteins/blood , Phosphorylation , Random Allocation , Soluble Guanylyl Cyclase/blood
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