What you need to know
- It is a longstanding cultural norm to provide supplemental oxygen to sick patients regardless of their blood oxygen saturation
- A recent systematic review and meta-analysis has shown that too much supplemental oxygen increases mortality for medical patients in the hospital
- For patients receiving oxygen therapy, aim for peripheral capillary oxygen saturation (SpO2) of ≤ 96% (strong recommendation)
- For patients with acute myocardial infarction or stroke, do not initiate oxygen therapy in patients with SpO2 ≥ 90% (for ≥ 93% strong recommendation, for 90-92% weak recommendation)
- A target SpO2 range of 90-94% seems reasonable for most patients and 88-92% for patients at risk of hypercapnic respiratory failure; use the minimum amount of oxygen necessary
Colours correspond to Class of Recommendation.
*Atropine should not be given in patients after
†In patients with drug toxicity and severe symptoms, preparation for pacing should proceed simultaneously with pharmacologic treatment of drug toxicity.
AADs indicates antiarrhythmic drugs; AV, atrioventricular;BB, beta blocker; CCB, calcium channel blocker; COR, Class of Recommendation;ECG, electrocardiographic; H+P, history and physical examination; IMI, inferior myocardial infarction; IV, intravenous; PM, pacemaker; S/P, status post; and VS, vital signs.
- Autonomic derangements during an acute MI are common, and small case series suggest that atropine can be used to increase heart rate. Atropine appears to be safe in those patients with
atrioventricular nodalblock in the absence of system disease. infranodalconduction
- In contrast, it is important to recognize that the use of atropine in patients with
disease or block can be associated with exacerbation of block and is infranodalconduction potentiallyof harm. Aminophylline/theophylline has also been examined in this setting, and in the context of very limited data appears likely to be safe if atropine is ineffective. The methylxanthines theophylline and aminophylline (a theophylline derivative) exert positive chronotropic effects on the heart, likely mediated by inhibition of the suppressive effects of adenosine on the sinoatrial node.
- Given that the natural course of
a MIwith conduction system abnormalities is frequently associated with recovery of conduction – early and unnecessary pacing should be avoided.
- Hyperacute T-waves are often the first manifestation of complete vessel occlusion; they are wide, bulky and prominent.
- Hyperacute T-waves are not necessarily tall, and small T-waves can still be hyperacute when paired with a low-amplitude QRS complex.
- De Winter T-waves represent LAD occlusion (a STEMI equivalent) requiring immediate revascularization.
- Previously inverted T-waves can appear normal and upright in the setting of acute vessel occlusion. This is known as pseudonormalization.
- The tall T-waves associated with hyperkalemia are sharp, pointy, symmetric, and have a narrow base.
- When in doubt, get serial ECGs (every 15 minutes) and use adjunctive information.
- The risk of ACS in patients with negative biomarkers and normal ECGs approaches 0.2%.
- Prior risk scores, such as TIMI and GRACE, provide little, if any benefit, in risk stratification for ED chest pain patients.
- The HEART score and pathway can risk stratify patients into three separate categories: low (0-3), moderate (4-6), and high score (> 7).
- Low-risk patients on the HEART pathway demonstrate likelihood of ACS that approaches < 1%, and it is easy to use in the ED.
- Risk factors, history, ECG, troponin, follow up, gestalt, patients with points 3 or 4, and research design are areas of potential weakness.
- Further improvement of the HEART pathway at this time is difficult, but in patients at moderate risk, CCTA may hold promise for evaluation of risk. This requires further study.
A cohort of 446 763 individuals including 61 460 with acute myocardial infarction was acquired. Taking any dose of NSAIDs for one week, one month or more than a month was associated with an increased risk of myocardial infarction. With use for one to seven days, the probability of increased myocardial infarction risk (posterior probability of odds ratio >1.0) was 92% for celecoxib, 97% for ibuprofen, and 99% for diclofenac, naproxen, and rofecoxib. The corresponding odds ratios (95% credible intervals) were 1.24 (0.91 to 1.82) for celecoxib, 1.48 (1.00 to 2.26) for ibuprofen, 1.50 (1.06 to 2.04) for diclofenac, 1.53 (1.07 to 2.33) for naproxen, and 1.58 (1.07 to 2.17) for rofecoxib. Greater risk of myocardial infarction was documented for the higher dose of NSAIDs. With use for longer than one month, risks did not appear to exceed those associated with shorter durations.