Effectiveness of platelet inhibition on major adverse cardiac events in non-cardiac surgery after percutaneous coronary intervention: a prospective cohort study.

BACKGROUND: Platelet inhibition is mandatory therapy after percutaneous coronary intervention (PCI). Withdrawal of oral antiplatelet agents has been linked to increased incidence of postoperative adverse cardiac events in post-PCI patients having non-cardiac surgery (NCS). There is limited knowledge of temporal changes in platelet inhibition in this high-risk surgical population. We therefore performed a multicentre prospective cohort study evaluating perioperative platelet function and its association with postoperative major adverse cardiac events (MACE). METHODS: In 201 post-PCI patients having NCS, we assessed the association between platelet function and postoperative MACE. We performed perioperative platelet function testing using a platelet mapping assay (PMA). Troponin-I was measured every 8 h for 2 days, then daily until day 5. Myocardial infarction was assessed using the third universal definition. We used multivariable logistic regression to assess the association between platelet inhibition and MACE. RESULTS: Major adverse cardiac events occurred in 40 patients within 30 days of surgery. Thirty-two of these events were non-ST-elevation myocardial infarction, four ST-elevation myocardial infarction, and four exacerbation of congestive heart failure. We were unable to show an association between platelet inhibition and MACE. The PMA showed declining levels of platelet inhibition the longer the antiplatelet therapy was withheld before surgery. Logistic regression did not show an association between preoperative platelet function or the type of stent and MACE. We found an increased cardiac risk of MACE after surgery within 6 weeks of PCI. CONCLUSIONS: The incidence of MACE in patients undergoing NCS after previous PCI is high in spite of adequate perioperative antiplatelet therapy. CLINICAL TRIAL REGISTRATION: NCT 01707459 (registered at http://www.clinicaltrials.gov).

Post-operative hypercapnia-induced hyperpnoea accelerates recovery from sevoflurane anaesthesia: a prospective randomised controlled trial.

BACKGROUND: The time to recovery from vapour anaesthesia is shortened by an increase in ventilation while maintaining normocapnia. Hypercapnia during emergence from anaesthesia in spontaneously breathing patients also increases anaesthetic clearance from the brain by increasing cerebral blood flow. We hypothesised that hypercapnia-induced hyperpnoea accelerates emergence from sevoflurane anaesthesia compared to the standard anaesthesia protocol. METHODS: After Ethics Review Board approval, 44 ASA I-III patients undergoing elective gynaecological surgery were randomised after surgery to either hypercapnic hyperpnoea or control groups. In the hypercapnic hyperpnoea group, the end-tidal CO2 was adjusted to a range of 6.0-7.3 kPa to maintain a minute ventilation of 10-15 l/min. Recovery indices were compared using unpaired t-tests and ANOVA. RESULTS: Prior to extubation, minute ventilation and end-tidal CO2 in hypercapnic hyperpnoea and control groups were 10.3 ± 1.7 l/min vs. 5.4 ± 1.2 l/min (P < 0.001) and 6.6 ± 0.6 kPa and 5.2 ± 0.5 kPa (P < 0.001), respectively. Compared to control, the study group had shorter time to extubation [4.4 ± 1.3 (SD) vs. 9.8 ± 4.4 min, P < 0.01], BIS recovery to > 75 (2.4 ± 0.9 vs. 6.1 ± 3.1 min, P < 0.01), eye opening (3.9 ± 1.6 vs. 9.8 ± 6.2 min, P < 0.01), eligibility for leaving operating room (5.1 ± 1.2 vs. 11.1 ± 4.6 min, P < 0.01), and post-anaesthesia care unit (73.9 ± 14.2 vs. 89.4 ± 22.6) CONCLUSION: Hypercapnic hyperpnoea in spontaneously breathing patients halves the time of recovery from sevoflurane-induced anaesthesia in the operating room.

Storage of strain-specific rat blood limits cerebral tissue oxygen delivery during acute fluid resuscitation.

BACKGROUND: The effect of blood storage on tissue oxygen delivery has not been clearly defined. Some studies demonstrate reduced microvascular oxygen delivery, whereas others do not. We hypothesize that storage of rat blood will limit its ability to deliver oxygen to cerebral tissue. METHODS: Anaesthetized rats underwent haemorrhage (18 ml kg(-1)) and resuscitation with an equivalent amount of fresh or 7 day stored strain-specific whole blood. Arterial blood gases, co-oximetry, red cell counts and indices, and blood smears were performed. Hippocampal tissue oxygen tension (PBr(O2)), regional cerebral blood flow (rCBF), and mean arterial pressure (MAP) were measured before and for 60 min after resuscitation (n=6). Data [mean (SD)] were analysed by anova. RESULTS: After 7 days, there was a significant reduction in pH, Pa(O2), an increase in Pa(CO2), but no detectable plasma haemoglobin in stored rat blood. Stored red blood cell morphology demonstrated marked echinocytosis, but no haemolysis in vitro. MAP and PBr(O2) in both groups decreased after haemorrhage. Resuscitation with stored blood returned MAP [92 (SD 16) mm Hg] and PBr(O2) [3.2 (0.7) kPa] to baseline, whereas rCBF remained stable [1.2 (0.1)]. Resuscitation with fresh blood returned MAP to baseline [105 (16) mm Hg] whereas both PBr(O2) [5.6 (1.5) kPa] and rCBF [1.9 (0.4)] increased significantly (P<0.05 for both, relative to baseline and stored blood group). There was no evidence of haemolysis in vivo. CONCLUSIONS: Although resuscitation with stored blood restored cerebral oxygen delivery to baseline, fresh blood produced a greater increase in both PBr(O2) and rCBF. These data support the hypothesis that storage limits the ability of RBC to deliver oxygen to brain tissue.