From the original EMS systems in Miami, Columbus and Pittsburgh that brought hospital-level cardiac care to the field, to today’s multi-lead ECG acquisition, prehospital fibrinolytic therapy, cardiac biomarker measurement and destination decisions, the role of the field care provider to assess and treat acute coronary syndrome has evolved considerably.
The 2015 American Heart Association Guidelines for Emergency Cardiac Care has several references for out of hospital ACS treatment that refines, and in some cases, defines the current state of the art — and science — of prehospital ACS care.
What is ACS?
Acute coronary syndrome is an umbrella term used to describe the variety of myocardial conditions that result from a sudden reduction of blood flow through the coronary arteries supplying oxygen and nutrients to heart muscle. This includes unstable angina as well as acute myocardial infarction.
An essential goal of ACS therapy is rapid reperfusion — opening a coronary artery that is suddenly blocked, usually by a thrombus which is a clot. An occluded artery cannot transport nutrients and oxygen to myocardial cells beyond the block, causing those cells to become ischemic. If uncorrected, ischemic myocardial cells will become injured and eventually die — an infarct. Depending on which type of injury — thrombus or infarct, and how long an artery is blocked will determine the location and extent of a myocardial infarction.
Reperfusion therapy happens in two ways. The thrombus can either be lysed, which is to dissolve with a fibrinolytic drug, such as Activase (alteplase) and Retavase (reteplase) or mechanically removed through percutaneous coronary intervention, or coronary angioplasty. While fibrinolytic therapy has become commonplace across the country, PCI must be done in centers where the equipment and expertise is available to perform the procedure.
Prehospital use of 12 lead ECGs
It is clear that the sooner a potential AMI is identified, the sooner reperfusion therapy can be instituted. Paramedics play a critical role in reducing door-to-balloon by identifying STEMIs — ST segment elevation myocardial infarctions -through the use of 12-lead ECGs [1, 2].
The AHA has identified prehospital 12-lead use as an effective tool in shortening the time it takes to achieve reperfusion. Identifying STEMIs in the field allows the paramedic to notify the receiving hospital early, as well as transport the patient to a facility capable of PCI if available. PCI has been shown to have better outcomes for STEMI patients when compared to fibrinolytic therapy.
Computerized 12-lead ECG interpretation
Studies have shown that computer interpretation of 12-lead ECGs have an unacceptably high false negative rates — that is, under diagnosing a STEMI. Because of this, it is not recommended to use computer interpretation of 12-lead ECGs alone when trying to determine the presence of a STEMI. It is appropriate to use it in conjunction with professional interpretation and judgement. Paramedics have been shown to have the same degree of accuracy as physicians in identifying STEMIs on a 12-lead ECG [3, 4].
Be cautious with supplemental oxygen
The routine use of supplemental oxygen for AMI patients with normal oxygen saturation levels has shown to be harmful [5, 6]. Avoid the administration of oxygen to patients with SpO2 readings greater than 94 percent.
Aspirin administration still recommended
Administering aspirin as soon as a possible after an AMI is identified continues to be a strong AHA recommendation, unless the patient has a known aspirin allergy or active gastrointestinal bleeding. The recommended aspirin dose is 160 to 325 mg, and it should be chewed and not swallowed whole in order to enter the bloodstream more rapidly.
Prehospital anticoagulant use
At this time there is not a recommendation for or against the use of prehospital anticoagulant use, such as heparin. EMS systems that have anticoagulant protocols should continue to monitor their use, while systems that do not have such interventions should not consider deploying them [7].
Nitroglycerin – no evidence but still use it
There is still no conclusive evidence for the routine use of nitroglycerin for AMI patients. The AHA continues to recommend the use of sublingual nitroglycerin for patients with signs of an AMI, with normotensive blood pressures, and no evidence of phosphodiesterase inhibitor use within 24 to 48 hours, depending upon which inhibitor was used.
Prehospital fibrinolytic use
While it has been shown that paramedics can safely administer fibrinolytic therapy in the field, it’s been questioned whether there is benefit to its use where transport times are short and access to PCI centers are readily available [8]. The AHA recommends that it is reasonable to administer prehospital fibrinolytics if transport times are greater than 30 minutes [9].
Transport to a PCI center after ROSC
Studies show that STEMI patients who achieve ROSC after cardiac arrest have better survival rates if they undergo PCI within 24 hours of the arrest [10]. EMS providers should transport out of hospital cardiac arrests to the nearest PCI center if available.
EMS providers regularly encounter patients with chest pain making it important to stay current on ACS assessment and treatment guidelines.
References
1. Davis M, Lewell M, McLeod S, Dukelow A. A prospective evaluation of the utility of the prehospital 12-lead electrocardiogram to change patient management in the emergency department. Prehosp Emerg Care. 2014;18:9–14.
2. Nam J, Caners K, Bowen JM, Welsford M, O’Reilly D. Systematic review and meta-analysis of the benefits of out-of-hospital 12-lead ECG and advance notification in ST-segment elevation myocardial infarction patients. Ann Emerg Med. 2014;64:176–86, 186.e1.
3. Feldman JA, Brins eld K, Bernard S, White D, Maciejko T. Real-time paramedic compared with blinded physician identification of ST-segment elevation myocardial infarction: results of an observational study. Am J Emerg Med. 2005;23:443–448.
4. Trivedi K, Schuur JD, Cone DC. Can paramedics read ST-segment elevation myocardial infarction on prehospital 12-lead electrocardiograms? Prehosp Emerg Care. 2009;13:207–214.
5. Kilgannon JH, Jones AE, Shapiro NI, Angelos MG, Milcarek B, Hunter K, Parrillo JE, Trzeciak S; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Association between arterial hyperoxia fol- lowing resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010;303:2165–2171.
6. Janz DR, Hollenbeck RD, Pollock JS, McPherson JA, Rice TW. Hyperoxia is associated with increased mortality in patients treated with mild therapeutic hypothermia after sudden cardiac arrest. Crit Care Med. 2012;40:3135–3139.
7. O’Connor RE et al. Part 9: Acute Coronary Syndromes: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015 Nov 3;132(18 Suppl 2):S483-500.
8. Welsh RC, Travers A, Senaratne M, Williams R, Armstrong PW. Feasibility and applicability of paramedic-based prehospital brinolysis in a large North American center. Am Heart J. 2006;152:1007–1014.
9. Idem, pg. S488.
10. Mooney MR, Unger BT, Boland LL, Burke MN, Kebed KY, Graham KJ, Henry TD, Katsiyiannis WT, Satterlee PA, Sendelbach S, Hodges JS, Parham WM. Therapeutic hypothermia after out-of-hospital cardiac arrest: evaluation of a regional system to increase access to cooling. Circulation. 2011;124:206–214.
