Perioperative myocardial ischemia and infarction are not only major sources of morbidity and mortality in patients undergoing surgery but also important causes of prolonged hospital stay and resource utilization. Ischemic and pharmacological preconditioning and postconditioning have been known for more than two decades to provide protection against myocardial ischemia and reperfusion and limit myocardial infarct size in many experimental animal models, as well as in clinical studies (1-3). This paper will review the physiology and pharmacology of ischemic and drug-induced preconditioning and postconditioning of the myocardium with special emphasis on the mechanisms by which volatile anesthetics provide myocardial protection. Insights gained from animal and clinical studies will be presented and reviewed and recommendations for the use of perioperative anesthetics and medications will be given.
Perioperative myocardial ischemia and infarction are not only major sources of morbidity and mortality in patients undergoing surgery but also important causes of prolonged hospital stay and resource utilization. Ischemic and pharmacological preconditioning and postconditioning have been known for more than 2 decades to provide protection against myocardial ischemia and reperfusion and limit myocardial infarct size in many experimental animal models, as well as in clinical studies. This article reviews the physiology and pharmacology of ischemic and drug-induced preconditioning and postconditioning of the myocardium with special emphasis on the mechanisms by which volatile anesthetics provide myocardial protection. Insights gained from animal and clinical studies are reviewed and recommendations given for the use of perioperative anesthetics and medications.
Objectives There are multiple published guidelines regarding comprehensive patient blood management, centered on the three pillars of patient blood management, manage preoperative anemia, minimize blood loss, and tolerate intra/postoperative anemia. We sought to create an order set to facilitate widespread implementation of evidence-based cardiac surgery patient blood management. Methods Subject matter experts were consulted to translate existing guidelines and literature into a sample turnkey order set for patient blood management. Orders derived from consistent Class I, IIA, or equivalent recommendations across referenced guidelines and consensus manuscripts appear in the TKO in bold type. Selected orders that were inconsistently Class I or IIA, Class IIB, or supported by published evidence, were also included in italicized type. Results Preoperatively there are strong recommendations to screen and treat preoperative anemia with iron replacement and erythropoietin, and to discontinue DAPT if the patient can safely wait for surgery. Intraoperative orders outline the routine use of an antifibrinolytic agent, cell saver, point of care viscoelastic testing, and use of a standard transfusion algorithm. The order set also reflects strong recommendations intraoperatively and postoperatively for agreed upon hemoglobin thresholds to consider transfusion of packed red blood cells. A hemoglobin threshold should be adopted according to local team consensus and should trigger a discussion regarding transfusion. Conclusion The benefit of a multidisciplinary PBM care pathway in cardiac surgery has been well established, yet implementation remains variable. Utilizing recommendations from existing guidelines, we have created a turnkey order set to facilitate the implementation of patient blood management. There are multiple published guidelines regarding comprehensive patient blood management, centered on the three pillars of patient blood management, manage preoperative anemia, minimize blood loss, and tolerate intra/postoperative anemia. We sought to create an order set to facilitate widespread implementation of evidence-based cardiac surgery patient blood management. Subject matter experts were consulted to translate existing guidelines and literature into a sample turnkey order set for patient blood management. Orders derived from consistent Class I, IIA, or equivalent recommendations across referenced guidelines and consensus manuscripts appear in the TKO in bold type. Selected orders that were inconsistently Class I or IIA, Class IIB, or supported by published evidence, were also included in italicized type. Preoperatively there are strong recommendations to screen and treat preoperative anemia with iron replacement and erythropoietin, and to discontinue DAPT if the patient can safely wait for surgery. Intraoperative orders outline the routine use of an antifibrinolytic agent, cell saver, point of care viscoelastic testing, and use of a standard transfusion algorithm. The order set also reflects strong recommendations intraoperatively and postoperatively for agreed upon hemoglobin thresholds to consider transfusion of packed red blood cells. A hemoglobin threshold should be adopted according to local team consensus and should trigger a discussion regarding transfusion. The benefit of a multidisciplinary PBM care pathway in cardiac surgery has been well established, yet implementation remains variable. Utilizing recommendations from existing guidelines, we have created a turnkey order set to facilitate the implementation of patient blood management.
Hyperglycemia is known to inhibit ischemic and anesthetic preconditioning. We tested whether hyperglycemia inhibits anesthetic postconditioning with isoflurane and whether this effect is mediated via phosphatidylinositol-3-kinase/Akt and nitric oxide signaling. New Zealand white rabbits subjected to 40 minutes of myocardial ischemia, followed by 3 hours of reperfusion were assigned to the following groups: ischemia and reperfusion (I/R), isoflurane (1 minimal alveolar concentration) postconditioning, and isoflurane postconditioning with hyperglycemia (15% dextrose in water infusion). A control group of hyperglycemia + I/R was also included. Levels of MB fraction of creatine kinase (CK-MB) were assessed as an indicator of myocardial damage, and infarct size was evaluated. Akt, iNOS, and endothelial nitric oxide synthase (eNOS) expression was assessed by immunoblotting. Determination of nitrite and nitrate levels in the myocardium was also performed. Isoflurane postconditioning reduced infarct size compared with the I/R group: 25% +/- 4% versus 49% +/- 5% (P < 0.01). CK-MB concentrations in the postconditioned animals (124% +/- 14% above baseline levels) were lower than those in the I/R group (236% +/- 9% above baseline levels; P < 0.01). Hyperglycemia inhibited the cardioprotective effect of isoflurane: myocardial infarction size was 46% +/- 4% and CK-MB increased to 241% +/- 11% above baseline. Phosphorylated Akt and eNOS protein expression increased after isoflurane postconditioning compared with the I/R group. These effects were also inhibited by hyperglycemia. iNOS expression, however, did not change significantly within the various experimental groups. There were increased tissue levels of nitrite and nitrate (NO(x)) in the postconditioning group. This was also blocked by hyperglycemia. Our results suggest that hyperglycemia inhibits cardioprotection provided by isoflurane postconditioning. This effect seems to be mediated via modulation Akt and eNOS.
We have assessed the effect of nebulised lignocaine, given pre‐operatively, upon the quality of induction of anaesthesia in cigarette smokers. Seventy‐five patients were studied in a double‐blind randomised fashion, receiving a nebuliser of either 4 ml 0.9% NaCl or 4 ml 4% lignocaine. All patients received a standardised anaesthetic consisting of thiopentone followed by progressive increments of enflurane. Thirty‐three out of 38 patients (87%) who received nebulised lignocaine had induction without adverse events, compared with 25 out of 37 patients (68%) in the nebulised saline group (Chi‐squared test p < 0.05). We conclude that the use of nebulised lignocaine, administered pre‐operatively, improves the quality of induction of anaesthesia in cigarette smokers.
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