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Context: International guidelines recommend the routine use of oxygen therapy in the treatment of myocardial infarction (MI). Objective: To undertake a systematic review and metaanalysis of randomised placebo-controlled trials of oxygen therapy in MI. Data sources: Medline, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, EMBASE and CINHAL. Study selection: Randomised placebo-controlled trials of oxygen therapy in MI. Data extraction: The primary clinical outcome was mortality. Results: Two of 51 potential studies met the inclusion criteria. The one study with substantive clinical outcome data reported that in uncomplicated MI, high-flow oxygen was associated with a non-significant increased risk of death (risk ratio 2.9, 95% CI 0.8 to 10.3, p = 0.08) and a greater serum aspartate aminotransferase level (difference 19.2 IU/ml, 95% CI 0 to 38.4, p = 0.05) than room air. Conclusion: The limited evidence that does exist suggests that the routine use of high-flow oxygen in uncomplicated MI may result in a greater infarct size and possibly increase the risk of mortality.Oxygen has been used in the treatment of myocardial infarction (MI) and acute coronary syndromes for over 100 years.1 The rationale for its longstanding use is that it increases oxygen delivery to the ischaemic myocardium, thereby reducing the size of the MI and improving clinical outcomes. Evidence in support of this approach is primarily derived from animal models, in which the administration of 100% oxygen under normobaric or hyperbaric conditions during and/or after experimental coronary artery occlusion reduces the extent of myocardial necrosis in some, 2-6 but not all, studies. 7-10However, concern has been expressed that the findings from animal studies may have poor generalisability to the clinical situation in humans. 11Furthermore, there is evidence that the routine use of high-flow oxygen in uncomplicated MI may not improve clinical outcomes and may potentially cause harm.11 12 It is well established that arterial oxygen tension is a major determinant of coronary artery tone [13][14][15][16] and that hyperoxia may result in a marked reduction in coronary artery blood flow. [17][18][19][20][21][22][23][24] Other cardiovascular effects of high-flow oxygen therapy include a reduction in cardiac output and stroke volume and an increase in systemic vascular resistance and blood pressure in patients with a MI. [25][26][27][28][29][30][31] Despite this conflicting evidence, contemporaneous international guidelines 32 33 recommend the routine use of supplemental oxygen in the treatment of MI. As the treatment of MI is at the forefront of evidence-based medicine, we sought to review the clinical efficacy and safety of the use of oxygen in this clinical situation. A systematic review was undertaken to identify randomised placebo-controlled trials of oxygen therapy in the treatment of acute MI with the intention of estimating differences in clinical outcomes by meta-analysis. METHODS Search strategyTo i...

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Background: Efforts to safely reduce length of stay for emergency department patients with symptoms suggestive of acute coronary syndrome (ACS) have had mixed success. Few system-wide efforts affecting multiple hospital emergency departments have ever been evaluated. We evaluated the effectiveness of a nationwide implementation of clinical pathways for potential ACS in disparate hospitals. Methods: This was a multicenter pragmatic stepped-wedge before-and-after trial in 7 New Zealand acute care hospitals with 31 332 patients investigated for suspected ACS with serial troponin measurements. The implementation was a clinical pathway for the assessment of patients with suspected ACS that included a clinical pathway document in paper or electronic format, structured risk stratification, specified time points for electrocardiographic and serial troponin testing within 3 hours of arrival, and directions for combining risk stratification and electrocardiographic and troponin testing in an accelerated diagnostic protocol. Implementation was monitored for >4 months and compared with usual care over the preceding 6 months. The main outcome measure was the odds of discharge within 6 hours of presentation Results: There were 11 529 participants in the preimplementation phase (range, 284–3465) and 19 803 in the postimplementation phase (range, 395–5039). Overall, the mean 6-hour discharge rate increased from 8.3% (range, 2.7%–37.7%) to 18.4% (6.8%–43.8%). The odds of being discharged within 6 hours increased after clinical pathway implementation. The odds ratio was 2.4 (95% confidence interval, 2.3–2.6). In patients without ACS, the median length of hospital stays decreased by 2.9 hours (95% confidence interval, 2.4–3.4). For patients discharged within 6 hours, there was no change in 30-day major adverse cardiac event rates (0.52% versus 0.44%; P =0.96). In these patients, no adverse event occurred when clinical pathways were correctly followed. Conclusions: Implementation of clinical pathways for suspected ACS reduced the length of stay and increased the proportions of patients safely discharged within 6 hours. Clinical Trial Registration: URL: https://www.anzctr.org.au/ (Australian and New Zealand Clinical Trials Registry). Unique identifier: ACTRN12617000381381.

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