Important studies and publications relevant to EMS providers are appearing at an ever increasing frequency. In this article, we review what we believe to be the five most important cardiovascular topics that have appeared in the literature over the past year.
They are: 1) new and emerging evidence on how and when to optimally provide therapeutic hypothermia; 2) the effectiveness of epinephrine in cardiac arrest; 3) the potential toxicity of oxygen in prehospital care; 4) optimal CPR techniques for the year 2015; and 5) incremental understanding on the role of prehospital ECGs.
1. Therapeutic Hypothermia
Since 2005, both the American Heart Association and the European Resuscitation Council have stated that therapeutic hypothermia (TH) is indicated for patients who survived cardiac arrest from v fib and v tach.1
Until recently, cooling to a temperature of 32—33 degrees C post cardiac arrest was considered the standard of care and a number of EMS systems were even beginning this therapy in the field prior to ED arrival. Two recent studies have begun to refine our understanding on the use and application of TH post cardiac arrest.
Study #1: The first article is a large multicenter European trial that compared “deep” TH at 33 degrees C to “mild” TH at 36 degrees C.2 The authors analyzed the results from 939 patients randomized to either of these temperatures.
The major finding of this article was that there was no benefit to cooling patients deeply to 33 degrees C vs. just cooling them mildly to 36 degrees C. At six month follow-up, 54% of the 33 degree C patient group had died or had a poor neurologic outcome (50% dead) vs. 52% of the 36 degree C patients (48% dead).
Of note, about 20% of the included patients from both groups had non-v fib/v tach arrest. There were no differences between the 33-degree C vs. 36-degree C cooled patients when each group’s patients were compared or when the non-v fib/v tach patients were compared.
Because this study prevented patients from developing a fever in either group for the first three days of the study, the authors have now begun to question whether TH is as important as preventing hyperthermia post arrest. At the present time, however, this reasoning that TH isn’t effective and that only fever prevention makes a difference, is purely speculative.
What does appear to be true is that TH doesn’t need to be as deep as first thought and that mildly cooling a patient to just 36 degrees C may be all that is requested.
Giving oxygen, especially by a 100% non-rebreather mask or 100% O2 by endotracheal tube, won’t change the O2 saturation but can raise O2 tensions by hundreds of mmHg.
Study #2: The second major study to appear in the past year comes from Seattle and King County, Wash.3 Researchers from the University of Washington evaluated whether beginning TH immediately post cardiac arrest in the field provided added benefits vs. awaiting in-hospital initiated therapy.
They randomized 1,359 patients over a five-year period to either EMS-begun TH or standard prehospital post-arrest care to 583 status/post (s/p) v fib patients and 776 non-shockable rhythm arrest patients, all of whom had return of spontaneous circulation (ROSC) but weren’t awake and responsive.
The authors found no benefit to the early, in-the-field initiation of TH by EMS providers vs. those who had TH begun after hospital arrival. Patients who received up to 2,000 cc of EMS-administered normal saline that had been cooled to 4 degrees C, had no better outcomes than those patients who received no EMS cooling.
A nearly identical 62.7% of the prehospital cooled s/p v fib patients were discharged versus 64.3% of the s/p v fib non-cooled EMS patients. There was no benefit seen in the non-v fib patient subgroups and no neurological benefits were seen in those patients who were cooled in the field.
Thus, even though the EMS-cooled patients arrived at the hospital with a reduced core temperature of more than 1 degree C compared to non-cooled patients and took one hour less to achieve targeted TH core temperatures, they had no improved survival or improved neurological outcomes.
It should also be noted that prehospital cooling was associated with increased rearrests during EMS transport and an increased incidence of pulmonary edema during the first hospital day.
Thus, as we approach 2015, the exact role of TH has become somewhat unclear. It appears that starting TH in the field offers no benefit in EMS systems with the relatively short transport times seen in typical urban and suburban systems. Once s/p v fib/v tach patients reach the hospital, if they have ROSC but can’t respond meaningfully, TH is indicated and likely needs to be at only 36 degrees C.
It’s not currently clear if there’s any benefit to deeper TH at 32—33 degrees C and some are now questioning if TH is beneficial or merely preventing fever s/p arrest. Finally, regardless of what temperature is used for comatose survivors of v fib/v tach, our strong bias is that all s/p v fib/v tach arrest patients who obtain ROSC should rapidly go to the cardiac catheterization laboratory regardless of whether their ECGs show an ST elevation myocardial infarction (STEMI) or not.4
2. Epinephrine in Cardiac Arrest
The role and efficacy of epinephrine has begun to be questioned. Although it has been central to the therapy of pulseless patients in cardiac arrest, its true value has never been rigorously studied in large, randomized, placebo-controlled human trials.
Study #1: Between the years of 2007—2010, the Japanese performed a large study in an attempt to answer the question as to the benefit of epinephrine in prehospital cardiac arrest.5
Studying all witnessed cardiac arrests in the entire nation over the time period, they compared outcomes of patients who received epinephrine vs. those who didn’t receive epinephrine. There were almost 2,000 pairs of patients with an initial rhythm of v fib/v tach who did and didn’t receive epinephrine, as well as almost 10,000 pairs with an initial rhythm of pulseless electrical activity (PEA) or asystole.5
The study found that there was increased ROSC with the prehospital administration of epinephrine in v fib/v tach (17% vs.13.4%), however, and likely more important, there was no increase in neurologically intact survival at discharge. This again stresses the importance of early defibrillation and high-quality CPR in v fib/v tach arrest as opposed to a priority on the administration of adrenaline in arrest.
When PEA and asystole were studied, results were predictably dismal. The prehospital administration of epinephrine did improve ROSC as with v fib/v tach (4% vs. 2.4%), but only improved neurologically intact survival at one month by 0.3% (0.7% vs. 0.4%).
Study #2: In another study looking at epinephrine’s efficacy, physicians and scientists in Australia noted there was little evidence epinephrine improved neurologically intact survival in cardiac arrest patients, so they also embarked on a randomized, double-blind, placebo-controlled trial to test this medication’s efficacy.6
This type of trial is considered the highest quality in research. Over the course of the study period, 262 patients received 1 mg of placebo during prehospital ACLS resuscitation and 272 received actual epinephrine. This study demonstrated that there was an increase in ROSC when epinephrine was given. However, looking downstream, there was no difference in survival to hospital discharge in patients receiving epinephrine or placebo by prehospital providers.
In another study, researchers analyzed all prehospital studies currently available that used standard epinephrine, high dose epinephrine or vasopressin in cardiac arrest.7 There were 14 studies included with more than 12,000 patients. There was no survival to discharge benefits or neurologic outcome differences in any group studied.
Thus, at the present time, epinephrine’s exact role and effectiveness remains unclear. However, following the current ACLS recommendation seems most prudent, until there’s consensus on changing its current dose, role or when to administer it. Perhaps, as noted below, adding additional medications to epinephrine is the answer.
It’s important to remember that CPR is a team endeavor and requires leadership and clearly defined roles in order to maximize performance.
Other treatment options in cardiac arrest: So, if epinephrine doesn’t provide significant benefits in cardiac arrest when used alone, are there any promising treatment options for EMS providers? Scientific theory suggests that vasopressin and steroid administration may provide protection of the brain in cardiac arrest, which epinephrine alone cannot accomplish.
Recently, a Greek study evaluated the administration of vasopressin, steroids and epinephrine (VSE) in a bundle during cardiac arrest.8 Of the more than 250 patients receiving this therapy compared to traditional treatment, VSE therapy resulted in increased ROSC as well as increased survival to discharge (13.9% vs. 5.1%).
Although these were inpatients, this is very promising research and may become standard of care in the near future for resuscitation.
3. Oxygen Therapy
For years oxygen has been the standard therapy for critically ill patients encountered in the prehospital setting. However, based on recent literature, it’s time to rethink the routine application of high-flow oxygen to non-hypoxemic patients in cardiac and non-cardiac emergencies. Not only does raising the PaO2 have little to no benefit on oxygen delivery when hemoglobin is already fully saturated, but hyperoxia can also deleteriously alter hemodynamics.
Hyperoxia is defined as a blood oxygen tension significantly above normal. Blood that’s 100% saturated at room air has an oxygen tension of about 100 mmHg. Giving oxygen, especially by a 100% non-rebreather mask or 100% O2 by endotracheal tube, won’t change the O2 saturation but can raise O2 tensions by hundreds of mmHg.
Hyperoxia, especially above 300—350 mmHg, can result in the formation of reactive oxygen species which can trigger inflammation and worsen reperfusion injury. This is true for a myriad of conditions including acute myocardial infarction, stroke, traumatic brain injury, chronic obstructive pulmonary disease (COPD) and cardiac arrest.
In patients suffering from acute myocardial infarction, hyperoxia can increase systemic vascular resistance while at the same time decreasing cardiac output and stroke volume.9 These effects worsen coronary blood flow and further impair oxygen delivery to the cardiac microcirculation.
It’s also been shown that patients who suffer sudden cardiac arrest have increased mortality and worse neurologic outcome when ROSC is achieved if they’re exposed to supra-normal oxygen levels.10 This may again be a result of cerebral and myocardial vasoconstriction or the contribution of hyperoxia to the post cardiac arrest syndrome.
Based on these findings, EMS providers should be sure patients with chest pain or ECG changes consistent with ischemia or infarction have their O2 saturations titrated into the mid-90s, but not aim for saturation levels of 98—100% . We should all certainly avoid high-flow O2 by mask in patients with good oxygen saturation to begin with.
Just like in cardiac patients, hyperoxic-induced vasoconstriction can also worsen oxygen delivery to damaged tissue in the brain. This, coupled with the formation of oxygen free radicals, can worsen outcome in patients suffering from stroke or traumatic brain injury.11—13
Rincon and colleagues recently evaluated how different levels of oxygenation can affect acute cerebrovascular accident (CVA) patients who had suffered an ischemic stroke, hemorrhagic stroke or subarachnoid hemorrhage.
They divided these CVA patients into three groups: hyperoxic; hypoxic and normal oxygen tension. They found that mortality with abnormal oxygenation was increased vs. those patients with normal oxygenation.
Mortality was 60% in the hyperoxic group, 53% in the hypoxic group and 47% in those with normal oxygenation. Surprisingly, mortality was higher with very high oxygen tensions than in hypoxic patients and hyperoxia was an independent predictor of death.
Another common situation in which oxygen is reflexively administered and not often carefully monitored is in the patient with respiratory distress from COPD. It’s understandable why this occurs, as patients with severe COPD often exhibit significant air hunger and high-flow oxygen seems appropriate. While this patient population is at risk for hypoxia, there’s also legitimate risk from hyperoxia as a result of the administration of 100% oxygen, as is commonplace.
In 2010, Austin and colleagues compared high flow oxygen with titrated oxygen in the treatment of patients with presumed COPD exacerbations in the prehospital setting.14
This study demonstrated a mortality rate of 2% in patients with COPD who were treated with titrated oxygen (target O2 sat of 88—92%) vs. 9% with standard high-flow O2. This more than four-fold increase in mortality is likely the result of hyperoxia diminishing the hypoxic respiratory drive in patients with COPD.
This increase in oxygenation depresses respirations, resulting in hypercarbia and respiratory acidosis. It may also increase
ventilation-perfusion mismatch in patients already in respiratory distress.
It’s therefore crucial that EMS providers pay close attention to how much oxygen critically ill patients receive in the prehospital setting.
The time for the blind administration of oxygen has passed and we strongly believe that EMS providers should target an oxygen saturation of approximately 94—95% and 89-92% for those with severe COPD.
Despite advances in technology and drug therapies, survival rates for out of hospital cardiac arrest in the U.S. remain dismal, with less than a 15% overall survival rate.15 Studies have consistently shown that high-quality CPR improves survival.15—17
By focusing on the delivery of high-quality CPR, many EMS systems have made dramatic improvements in neurologically intact survival rates.
The American Heart Association has identified five critical components of high-quality CPR:
- Chest compression fraction (CCF): Chest compression fraction is the proportion of time chest compressions are performed during the cardiac arrest. The goal of CCF is at least 80%, therefore it is essential to minimize interruptions of chest compressions.
- Chest compression rate: 100—120 compressions per minute is the optimal manual compression rate in both adults and children. Anything above or below this range will decrease cardiac output, coronary perfusion and, ultimately, neurologically intact survival.
- Chest compression depth: Compression depths of 2 inches (50mm) in adults, and 1/3 the chest anterior-posterior dimension in infants and children are the minimum compression depths needed to ensure optimal CPR efficacy.
- Full chest recoil: It’s essential not to lean on the chest during recoil so that full re-expansion of the chest cavity and lungs can occur. This will maximize venous return during relaxation and allow maximal cardiac output during compression.
- Avoid excessive ventilation: By delivering between 6—12 breaths per minute, the lungs aren’t expanded for much of the compression fraction. Thus, the less the lungs are expanded, the more blood will be returned to the heart. Positive pressure ventilation lowers cardiac output, therefore tidal volumes need only to produce a small visible rise in the chest wall.
The recent literature has demonstrated that the consistent delivery of high-quality CPR requires constant performance monitoring and feedback. Even well-trained providers fail to consistently deliver high-quality CPR. Systemic continuous quality improvement programs should be implemented to monitor CPR quality and resuscitation outcomes.
Remember the adage: “If you don’t measure it, you can’t improve it.”15 CPR is a team endeavor and CPR performance is enhanced when team members have a designated leader and clearly defined roles.
Strong team leadership requires orchestration of tasks with the focus toward delivering high-quality CPR. All tasks requiring interruption of chest compressions should be done simultaneously, modeling the “pit crew” teams in
Recent studies have also demonstrated the importance of the “peri-shock pause” and rates of survival after a cardiac arrest.16, 17
The “peri-shock pause” is defined as the time interval from the cessation of compressions to the time of defibrillation (pre-shock time) plus the time from shock to resumption of chest compressions (post-shock time).
Limiting the pre-shock interval to less than 10 seconds and the peri-shock interval to less than 20 seconds improves outcomes. There was an approximate 50% increase in survival when the pre-shock pause was less than 10 seconds as compared to those whose pre-shock pause was greater than 20 seconds.2
Interestingly, the length of the post-shock interval has not been found to play a role in survival. The pre-shock pause can be shortened by pre-charging the manual defibrillator during the last five seconds of the CPR cycle before the rhythm check. This will eliminate the time needed to charge the defibrillator after a shockable rhythm is detected.
In a recently published study, doing compressions while the machine was charging decreased the pre-shock pause from 15 to 3.5 seconds and improved the compression fraction by almost 10%.17
When using an AED, compressions during charging will decrease the peri-shock pause. Unfortunately, the ability for the AEDs to reliably interpret a rhythm and charge during compressions isn’t yet widely available.
In summary, there are five critical components of manual CPR that help to define the delivery of high-quality care during a cardiac arrest. It’s also important to remember that CPR is a team endeavor and requires leadership and clearly defined roles in order to maximize performance.
Continuous monitoring and feedback on CPR performance is essential. Recent studies have illustrated that strategies geared toward limiting the peri-shock pause improve survival.
5. Prehospital ECGs
Obtaining and interpreting prehospital ECGs is an essential skill for a paramedic, yet sensitivity and specificity among different EMS systems varies for identifying STEMI. Many systems use paramedic interpretation, often coupled with automated interpretation of the ECG, while others also include transmission to base station for physician interpretation.
Studies have found that paramedics are best at interpreting inferior STEMI (96%), followed by anterior STEMI (78%); however, only about 51% correctly recognized a lateral STEMI.21 (See Figure 1, below).
Although paramedics continue to be more expert in recognizing STEMIs, there’s the potential for falsely labeling STEMI mimics, such as bundle branch blocks, LVH and paced rhythms as STEMIs,21 as well as failing to recognize hyper-acute T waves, Wellen’s syndrome and posterior STEMIs.18
Based on these findings, we believe all EMS systems should focus on teaching their paramedics to become experts in reading ECGs for STEMIs and also to transmit ECGs to the receiving hospital for physician review. Rather than focusing on all STEMI patterns, including high lateral, posterior and right ventricular, a recent article demonstrated that prehospital STEMIs are mostly composed of inferior (55%) and anterior (41%) patterns, and educational efforts should be focused on these two patterns.
We believe it’s pointless to debate whether systems should transmit their prehospital ECGs for STEMI confirmation, but believe strongly that systems should aim for optimal teamwork where paramedic ECG interpretation, computer ECG read and ED doctors all work together in deciding whether the PCI team should be activated.
Much more effort should be devoted to improving the number of STEMI patients who receive prehospital ECG, as a recent study showed that only 47—55% of STEMI patients brought in by EMS have an ECG recorded.24 The importance of prehospital ECGs cannot be overstated. In a recently published meta-analysis of 16 studies involving 14,000 patients, prehospital ECGs decreased mortality by 37% and reduced door-to-balloon times by between 21—78 minutes.25
Obtaining and potentially transmitting a prehospital ECG in patients with the potential for acute coronary syndrome (ACS) is important even when initial ECG doesn’t show STEMI.
In one study, 11% of patients who were eventually diagnosed with a STEMI initially had a nondiagnostic ECG.19 Of these patients, 72.4% developed STEMI on ECG within 90 minutes of initial ECG, underlying the importance of repeating ECGs during transport in patients with symptoms highly suspicious for ACS and, in particular, those patients whose symptoms change en route.19
Oppositely, between 3—22% of patients with initial STEMI on ECG may have resolution of ST-elevation by the time they get to the ED.20,23 This may be due to spontaneous reperfusion and/or prehospital treatments; however, these patients remain at high risk of reocclusion and should be treated as STEMI patients.
Even if patients don’t have a STEMI on initial ECG or by the time they get to the ED, prehospital ECGs have great value. In another recent study from Ontario, 281 prehospital ECGs of patients without STEMI were evaluated. Of these, 12.3% had clinically significant abnormalities that weren’t present by the time the patient arrived at the ED, such as ST depression, T-wave inversions or arrhythmias.22
Of these abnormalities, 65.7% changed physician management.22 Another 21 prehospital ECGs weren’t different than the initial ED ECG, but influenced patient management prior to obtaining initial ECG (such as early consultation or treatment). In this study, a total of 18.5% of prehospital ECGs changed or influenced ED physician management.22
In summary, prehospital ECGs are increasingly common and the expertise of interpretive skills of paramedics continues to increase. Systems should specifically focus on paramedic expertise in reading anterior and inferior
STEMIs, preferentially, as these two patterns are by far the most common STEMI patterns seen.
Optimal care is more likely when the paramedic, the computer and the ED physician are all interpreting the prehospital ECG as a team. And finally, the prehospital ECG has great value, even if it doesn’t show a STEMI, as it can be compared to the ED’s ECG and serial ones obtained later. One ECG begets another!
We close this article with five summary statements:
- Therapeutic hypothermia started in the prehospital setting doesn’t appear to have any proven benefits and once the patient arrives at the hospital, mild hypothermia to just 36 degrees C, rather than 32 degrees C, may become the new standard of care.
- Epinephrine’s role in CPR remains unproven and it may be that it’s more effective if combined with vasopressin and, perhaps, steroids.
- Oxygen isn’t a benign drug and EMS providers should aim for an O2 saturation of 94—95% in most critically ill patients, rather than 100%, and aim for just 89—92% in those patients with significant COPD.
- CPR needs to be performed meticulously well with a focus on minimizing the pre-shock pause by performing compressions during charging and adherence to a compression depth of at least 2 inches and a rate of 100—120 compressions per minute.
- The prehospital ECG has great value even if it doesn’t show a STEMI as it can be used for comparison purposes with one or more EMS or in-ED ECGs. “One ECG begets another.”
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