to eligible patients and monitoring aspirin administration through established quality assurance programs [34].
Varying doses of aspirin have been proposed, but for ACS the most widely used dose is four 81‐mg baby aspirin tablets. These tablets are well tolerated, easy to swallow, and more rapidly absorbed than other preparations. Rectal preparations (300 mg) should be considered in patients unable to swallow. Acceptable contraindications to aspirin administration include definitive aspirin allergy or a history of active gastrointestinal bleeding.
Nitroglycerin
Nitroglycerin is a time‐honored treatment to relieve chest pain due to angina by decreasing myocardial oxygen demand and increasing collateral blood flow to ischemic areas of the heart. Somewhat surprisingly, nitroglycerin is not effective at reducing STEMI patient mortality [35]. Also, the response, or lack thereof, to nitroglycerin administration is not an accurate diagnostic test to determine whether cardiac ischemia is the underlying cause of a patient’s chest pain [36]. For example, because it relaxes smooth muscle, nitroglycerin may also relieve pain in patients with esophageal spasm.
Nitroglycerin can be administered as sublingual tablets or an oral spray. The usual dose for either method of delivery is 0.4 mg. Although up to three doses can be given, at intervals of 5 minutes between doses, current AHA/ACC recommendations for self‐administered patient use of nitroglycerin is for people to call EMS if chest pain is not improved 5 minutes after single dose of nitroglycerin. In so doing, STEMI patients avoid a potential 15‐ to 20‐minute delay before activating the EMS system [15, 16].
Although there is no difference in the incidence of nitroglycerin‐induced hypotension between groups of patients with inferior versus noninferior wall STEMI, nitroglycerin should be avoided in several groups of patients with chest pain [37]. Patients who have used phosphodiesterase inhibitors and then take nitrates can have profound, refractory hypotension. Nitrates generally should be avoided for 24 hours following sildenafil or vardenafil use and for 48 hours following tadalafil use.
Patients with a right ventricular infarction are dependent on right ventricular filling pressure to maintain cardiac output and a normal systolic blood pressure. If the patient has a systolic blood pressure below 100 mmHg or a heart rate below 60 beats per minute, nitroglycerin should be avoided until a 12‐lead ECG, including right‐sided leads, documents the absence of a right ventricular infarction. Nitroglycerin should also be avoided or used with caution in patients who already have systolic blood pressures <90 mmHg or heart rates <50 or >100 beats per minute [38].
Opiate analgesics
A large retrospective case series of hospitalized patients with non‐ST segment elevation ACS found that patients who received morphine had a higher mortality than those who did not [39]. It is unclear whether this was a causal effect or simply indicated that those who required morphine may have had more severe disease. A possible mechanism of harm from opiate therapy may be an interaction between opiate administration and platelet reactivity [40]. The AHA/ACC treatment guidelines for patients with unstable angina or non‐ST‐elevation MI (NSTEMI) reduce the strength of recommendation for morphine from Class I to Class IIa for patients with non‐STEMI [41]. The 2013 AHA/ACC STEMI Guidelines give morphine a Class I recommendation in STEMI patients because those patients are going to have reperfusion therapy [16]. The recommended dose of morphine for the patient with chest pain is 2–4 mg intravenously with increments of 2–8 mg intravenously repeated at 5‐ to 15‐minute intervals when pain is not adequately controlled with nitroglycerin.
Morphine sulfate has traditionally been the treatment of choice for prehospital patients suspected of ACS/STEMI. A common prehospital alternative is fentanyl. A prospective, randomized, prehospital clinical trial found the latter to be a safe and effective alternative to morphine sulfate, resulting in similar analgesia with no significant difference in hypotension [42].
Beta‐Blockers
Older guidelines recommended IV beta‐blocker (typically metoprolol) administration early in the course of acute myocardial infarction because of data suggesting reduced rates of reinfarction and recurrent ischemia when patients received both fibrinolytics and IV beta‐blockers. A large placebo‐controlled randomized trial showed that the effect of beta‐blockers in reducing arrhythmic events is equally offset by an increase in development of cardiogenic shock, and survival is similar regardless of early administration of intravenous beta‐blockers [43]. Current AHA/ACC recommendations for administration of intravenous beta‐blockers in the setting of STEMI are limited to patients who are hypertensive or have ongoing ischemia with no contraindications to their use [16]. On balance, the guidelines suggest that the need for prehospital administration of beta‐blockers to patients with STEMI is limited.
Prehospital fibrinolysis
Since fibrinolytics were introduced to emergency cardiac care in the mid‐1980s, some have proposed initiating the drug in the prehospital setting. Several studies published in the early 1990s showed that the strategy was feasible and that it could decrease mortality from STEMI in settings that had relatively long EMS response and/or transport intervals [44, 45]. Additional studies reinforced the original findings. A meta‐analysis of pooled results from six randomized trials enrolling more than 6,000 subjects concluded that prehospital initiation of fibrinolytics decreased all‐cause mortality by shortening initiation of fibrinolytics by 58 minutes [46].
Prehospital fibrinolysis has not been used commonly in the United States compared to Europe, where there are often physician‐staffed ambulances [47]. However, even in Europe prehospital fibrinolysis has been replaced by primary PCI for treatment of STEMI. In a prospective observational cohort study of 26,205 consecutive patients with STEMI in Sweden, representing about 95% of the population of STEMI patients in the country, those who were treated with primary PCI had lower 30‐day mortality than those treated with fibrinolytics in the hospital (4.9% versus 11.4%) [48]. Primary PCI patients also had lower mortality than those treated with prehospital fibrinolytics (4.9% versus 7.6%).
Several large clinical trials examined the strategy of transferring patients to PCI‐capable institutions from local hospitals compared with administration of fibrinolytics at the local hospitals [49, 50]. For situations in which transfer directly to a center capable of primary PCI is not possible in a timely fashion, a strategy of fibrinolysis at a non‐PCI hospital followed by transport to a regional PCI center may be necessary.
Systems of care for STEMI
The EMS system plays a key role in shortening the process of caring for patients with STEMI. Patients who are transported by EMS have shorter treatment intervals than those patients who arrive at the hospital by other means [51]. Patients can be encouraged to use EMS appropriately. A community intervention to shorten the time interval from symptom onset to ED arrival was shown to increase the proportion of ACS patients who used EMS for transport to the ED, though no effect was seen on the time interval of interest [52].
Prehospital notification/field cardiac catheterization laboratory
Activation
A key benefit of a prehospital 12‐lead ECG is notification of the receiving facility of an impending STEMI patient’s arrival. Shortening door‐to‐balloon time by 30 minutes reduces in‐hospital mortality from STEMI by about 1% [53]. Implementation of a prehospital 12‐lead ECG program with prehospital notification shortened door‐to‐balloon times by about 60 minutes in San Diego [54]. An evaluation of a large patient registry revealed that prehospital notification and subsequent ED activation of the catheterization team, before patient arrival at the hospital, shortened door‐to‐balloon time by approximately 15 minutes [55].
Occasional false‐positive activation of the PCI team is a necessary by‐product of an aggressive field approach to alerting hospitals about patients with suspected STEMI. One report suggests that up to 15%–20% of team activations may not result in any intervention [56]. The rate