Accounting for Breakout in Britain: The Industrial Revolution Through a Malthusian Lens

Over the past few years non-cardiac surgery has been recognised as a serious circulatory stress test which may trigger cardiovascular events such as myocardial infarction, in particular in patients at high risk. Detection of these postoperative cardiovascular events is difficult as clinical symptoms often go unnoticed. To improve detection, guidelines advise to perform routine postoperative assessment of cardiac troponin. Troponin elevation – or postoperative myocardial injury – can be caused by myocardial infarction. However, also non-coronary causes, such as cardiac arrhythmias, sepsis and pulmonary embolism, may play a role in a considerable number of patients with postoperative myocardial injury. It is crucial to acquire more knowledge about the underlying mechanisms of postoperative myocardial injury because effective prevention and treatment options are lacking. Preoperative administration of beta-blockers, aspirin, statins, clonidine, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, and preoperative revascularisation have all been investigated as preventive options. Of these, only statins should be considered as the initiation or reload of statins may reduce the risk of postoperative myocardial injury. There is also not enough evidence for intraoperative measures such blood pressure optimisation or intensified medical therapy once patients have developed postoperative myocardial injury. Given the impact, better preoperative identification of patients at risk of postoperative myocardial injury, for example using preoperatively measured biomarkers, would be helpful to improve cardiac optimisation

An observational study of end-tidal carbon dioxide trends in general anesthesia

PURPOSE: Despite growing evidence supporting the potential benefits of higher end-tidal carbon dioxide (ETCO METHODS: This retrospective, observational, multicentre study included 317,445 adult patients who received general anesthesia for non-cardiothoracic procedures between January 2008 and September 2016. The primary outcome was a time-weighted average area-under-the-curve (TWA-AUC) for four ETCO RESULTS: Both TWA-AUC and median ETCO CONCLUSIONS: Between 2008 and 2016, intraoperative ETC

Cardiac events within one year after a subarachnoid haemorrhage : The predictive value of troponin elevation after aneurysm occlusion

Background: Patients who survive after an aneurysmal subarachnoid haemorrhage (ASAH) have an increased incidence of cardiovascular events compared with the general population. We assessed whether troponin elevation after aneurysm occlusion, as marker of myocardial injury, can predict long-term cardiac events. Methods: We analysed a prospectively collected cohort of 159 patients with ASAH and early aneurysm occlusion, in whom routine post-intervention troponin I (TnI) measurements were performed. With competing risk regression modelling we estimated the association between TnI elevation after aneurysm occlusion and major adverse cardiac events within one year. Secondary outcome measures were all-cause mortality and neurological condition within one year. The predictive value of post-intervention TnI was compared with the predictive value of pre-intervention characteristics using c-statistics and the integrated discrimination improvement index. Results: Subdistribution hazard ratios for TnI elevation and major adverse cardiac events at one year were 1.05 (95% confidence interval (CI) 1.03–1.07) per 10 ng/l increase in TnI and 7.91 (95% CI 1.46–43.0) for any TnI elevation. After adjustment for pre-intervention variables, the subdistribution hazard ratios were 1.47 (95% CI 0.81–2.67) per 10 ng/l and 9.00 (95% CI 1.62–50.1) for any elevation. The c-statistic was 0.71 for TnI elevation as a continuous measure and 0.69 for any TnI elevation. The integrated discrimination improvement index showed a minimum improvement in prediction of 0.08 (interquartile range 0.06 to 0.09) for TnI as a continuous measure and 0.003 (interquartile range −0.004 to 0.01) for any TnI elevation, when compared with pre-intervention characteristics. Conclusion: TnI elevation after occlusion of a ruptured intracranial aneurysm predicts the occurrence of a major adverse cardiac event within one year after ASAH

Blood Pressure and End-tidal Carbon Dioxide Ranges during Aneurysm Occlusion and Neurologic Outcome after an Aneurysmal Subarachnoid Hemorrhage

WHAT WE ALREADY KNOW ABOUT THIS TOPIC: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Hypocapnia, hypotension, and hypertension during aneurysm occlusion in patients with an aneurysmal subarachnoid hemorrhage may lead to a poor prognosis, but evidence for end-tidal carbon dioxide (ETCO2) and mean arterial pressure (MAP) targets is lacking. Within the ranges of standardized treatment, the authors aimed to study the association between hypocapnia (PaCO2 100 mmHg) during general anesthesia for aneurysm occlusion and neurologic outcome. METHODS: This retrospective observational study included patients who underwent early aneurysm occlusion after an aneurysmal subarachnoid hemorrhage under general anesthesia. ETCO2 and MAP were summarized per patient as the mean and time-weighted average area under the curve for various absolute (ETCO2 90, > 100 mmHg) and relative thresholds (MAP < 70%, < 60%, < 50%). Clinical outcome was assessed with the Glasgow Outcome Scale at discharge and at three months, as primary and secondary outcome measure, respectively. RESULTS: Endovascular coiling was performed in 578 patients, and 521 underwent neurosurgical clipping. Of these 1,099 patients, 447 (41%) had a poor neurologic outcome at discharge. None of the ETCO2 and MAP ranges found within the current clinical setting were associated with a poor neurologic outcome at discharge, with an adjusted risk ratio for any ETCO2 value less than 30 mmHg of 0.95 (95% CI, 0.81 to 1.10; P < 0.496) and an adjusted risk ratio for any MAP less than 60 mmHg of 0.94 (95% CI, 0.78 to 1.14; P < 0.530). These results were not influenced by preoperative neurologic condition, treatment modality and timing of the intervention. Comparable results were obtained for neurologic outcome at three months. CONCLUSIONS: Within a standardized intraoperative treatment strategy in accordance with current clinical consensus, hypocapnia, hypotension, and hypertension during aneurysm occlusion were not found to be associated with a poor neurologic outcome at discharge in patients with an aneurysmal subarachnoid hemorrhage

Effects of dobutamine and phenylephrine on cerebral perfusion in patients undergoing cerebral bypass surgery: a randomised crossover trial

BACKGROUND Patients undergoing cerebral bypass surgery are prone to cerebral hypoperfusion. Currently, arterial blood pressure is often increased with vasopressors to prevent cerebral ischaemia. However, this might cause vasoconstriction of the graft and cerebral vasculature and decrease perfusion. We hypothesised that cardiac output, rather than arterial blood pressure, is essential for adequate perfusion and aimed to determine whether dobutamine administration resulted in greater graft perfusion than phenylephrine administration. METHODS This randomised crossover study included 10 adult patients undergoing cerebral bypass surgery. Intraoperatively, patients randomly and sequentially received dobutamine to increase cardiac index or phenylephrine to increase mean arterial pressure (MAP). An increase of >10% in cardiac index or >10% in MAP was targeted, respectively. Before both interventions, a reference phase was implemented. The primary outcome was the absolute difference in graft flow between the reference and intervention phase. We compared the absolute flow difference between each intervention and constructed a random-effect linear regression model to explore treatment and carry-over effects. RESULTS Graft flow increased with a median of 4.1 (inter-quartile range [IQR], 1.7-12.0] ml min$^{-1}$) after dobutamine administration and 3.6 [IQR, 1.3-7.8] ml min$^{-1}$ after phenylephrine administration (difference -0.6 ml min$^{-1}$; 95% confidence interval [CI], -14.5 to 5.3; P=0.441). There was no treatment effect (0.9 ml min$^{-1}$; 95% CI, 0.0-20.1; P=0.944) and no carry-over effect. CONCLUSIONS Both dobutamine and phenylephrine increased graft flow during cerebral bypass surgery, without a preference for one method over the other. CLINICAL TRIAL REGISTRATION Netherlands Trial Register, NL7077 (https://www.trialregister.nl/trial/7077)

Postoperative myocardial injury phenotypes and self-reported disability in patients undergoing noncardiac surgery:a multicentre observational study

Background: Postoperative myocardial injury (PMI) comprises a spectrum of mechanisms resulting in troponin release. The impact of different PMI phenotypes on postoperative disability remains unknown. Methods: This was a multicentre prospective cohort study including patients aged ≥50 yr undergoing elective major noncardiac surgery. Patients were stratified in five groups based on the occurrence of PMI and clinical information on postoperative adverse events: PMI classified as myocardial infarction (MI; according to fourth definition), PMI plus adverse event other than MI, clinically silent PMI (PMI without adverse events), adverse events without PMI, and neither PMI nor an adverse event (reference). The primary endpoint was 6-month self-reported disability (assessed by WHO Disability Assessment Schedule 2.0 [WHODAS]). Disability-free survival was defined as WHODAS ≤16%. Results: We included 888 patients of mean age 69 (range 53–91) yr, of which 356 (40%) were women; 151 (17%) patients experienced PMI, and 625 (71%) experienced 6-month disability-free survival. Patients with PMI, regardless of its phenotype, had higher preoperative disability scores than patients without PMI (difference in WHODAS; β: 3.3, 95% confidence interval [CI]: 0.5–6.2), but scores remained stable after surgery (β: 1.2, 95% CI: –3.2–5.6). Before surgery, patients with MI (n=36, 4%) were more disabled compared with patients without PMI and no adverse events (β: 5.5, 95% CI: 0.3–10.8). At 6 months, patients with MI and patients without PMI but with adverse events worsened in disability score (β: 11.2, 95% CI: 2.3–20.2; β: 8.1, 95% CI: 3.0–13.2, respectively). Patients with clinically silent PMI did not change in disability score at 6 months (β: 1.39, 95% CI: –4.50–7.29, P=0.642).Conclusions: Although patients with postoperative myocardial injury had higher preoperative self-reported disability, disability scores did not change at 6 months after surgery. However, patients experiencing myocardial infarction worsened in disability score after surgery.</p

Kinetics of troponin I in patients with myocardial injury after noncardiac surgery

Background: Myocardial injury after noncardiac surgery, as measured by troponin elevation, is strongly associated with mortality. However, it is unknown in which patients prognosis can be improved. The presence of kinetic changes of troponin may be associated with a worse prognosis and warrant more aggressive management. Therefore, we aimed to study the kinetics of troponin in patients with postoperative myocardial injury, and to determine the added predictive value of kinetic changes of troponin on mortality. Methods: This cohort study included patients with myocardial injury after noncardiac surgery. Troponin I (TnI) was measured on the first three postoperative days. The primary outcome was all-cause 1-year mortality. We studied both absolute and relative TnI changes, and determined the delta TnI that was associated with mortality to distinguish a rise-and-fall TnI pattern from a stable TnI pattern. Next, we determined the added predictive value of a rise-and-fall TnI pattern for mortality. Results: In total, 634 patients were included. The risk ratio (RR) for mortality increased significantly with an absolute delta TnI of ≥ 200 ng/L (RR 1.5, 99.4% CI 1.0.2.2, p = 0.003). Using this delta TnI to define a rise-and-fall pattern, 459 patients (72%) had a stable TnI pattern and 175 patients (28%) had a rise-and-fall pattern. When added to a model including the highest TnI value and variables from the revised cardiac risk index (RCRI), the TnI pattern did not increase the predictive value for mortality. Conclusions: A postoperative TnI rise-and-fall pattern was associated with 1-year mortality, but had no added value in addition to the highest TnI level to predict 1-year mortality. Therefore, postoperative TnI kinetics are not useful for further mortality risk stratification in patients with myocardial injury after noncardiac surgery

Relationship Between Preoperative Evaluation Blood Pressure and Preinduction Blood Pressure : A Cohort Study in Patients Undergoing General Anesthesia

BACKGROUND:: For outcomes research where changes in intraoperative blood pressure are a possible causative factor, it is important to determine an appropriate source for a reference value. We studied to what extent preinduction blood pressure values in the operating room differ from those obtained during preoperative evaluation outside the operating room. METHODS:: Cohort study including 4408 patients aged 60 years or older undergoing noncardiac surgery. The outcome was the difference between the preinduction mean blood pressure (MBP) and the MBP obtained during preoperative evaluation. A difference of ≥10 mm Hg was considered clinically relevant. A paired samples t test was used to estimate the difference. Linear regression was used to obtain estimates adjusted for patient characteristics, comorbidity, medications, type of surgery, and preoperative blood pressure. RESULTS:: Complete data were available for 3660 (83%) patients. There were 2228 (61%) patients with a difference of ≥10 mm Hg between the preinduction and preoperative MBP. The overall mean difference between both MBPs was 11 mm Hg (95% confidence interval, 10–11) with important variability among individuals. Patients with higher preoperative MBP values had smaller differences. After adjusting for patient characteristics, comorbidity, medications, type of surgery, and preoperative blood pressure, the difference decreased an estimated 5.0 mm Hg (95% confidence interval, 4.7–5.4) for every increase of 10 mm Hg in preoperative MBP. Patient characteristics, comorbidity, type of surgery, or medication were not strongly associated with the difference. CONCLUSIONS:: The average preinduction blood pressure was higher than the preoperative blood pressure. This difference between the measurements can be explained by stress-induced effects and regression to the mean. To define an optimal reference value for research purposes or to arrive at a clinical perioperative blood pressure target, one should consider that there is important variability both within and between patients