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April 19, 2010
During a heart attack, your coronary supply line of oxygenated blood and nutrients is being choked off and if left untreated, may result in heart muscle death (myocardial infarction) that too often causes disability or death. The increased obstruction is caused by a blood clot that develops on a cholesterol plaque that has already narrowed the inside of one or more coronary arteries. As the blood clot grows, the heart muscle becomes less and less oxygenated, which produces the symptoms of heart ischemia.
The classic presentation is substernal chest pain and perhaps one or more typically associated symptoms, such as radiation of the chest pain to the neck or arms, shortness of breath, or sweating. Atypical presentations may include pain from the epigastric area, back or shoulder or no chest pain at all but with increasing fatigue or shortness of breath. So what's an EMT supposed to do?
If you suspect your patient's chest pain or presenting symptoms are coming from an oxygen poor or ischemic heart, you must assume that the patient is experiencing an acute coronary syndrome and should begin treatment with oxygen, aspirin, nitroglycerine and timely transport depending on your local protocols and medical direction. Then you need to determine whether the symptoms are from a partially blocked artery or a totally occluded artery, which does the most damage over the shortest period of time and requires rapid treatment to get rid of the clot. And you potentially have this tool in your rig.
Cardiac ischemia may produce changes on a 12- or 15-lead ECG that correspond to the area of the heart receiving inadequate blood flow. If the arterial blockage is incomplete, the ECG may show ST segment depression or changes in the T waves — or even be normal.
Further testing at a medical facility is needed to determine if these symptoms and ECG changes are due to unstable angina or a partial arterial obstruction producing a non-ST Segment Elevation Myocardial Infarct (NSTEMI). The initial goal for treatment of a NSTEMI is to prevent the partially obstructing clot from getting larger through treatment with medications that decrease platelet adhesion (such as aspirin and glycoprotein IIb llla inhibitors) and with heparin anticoagulation. Intravenous clot-busting drugs are ineffective in treating a NSTEMI and may even make it worse.
For the patient suffering from a complete occlusion of one or more coronary arteries, the severe ischemia causes ST segment elevation from the ECG leads reading the electrical activity from the affected area of the heart. Thus the term "ST Segment Elevation Myocardial Infarction (STEMI)" for a heart attack reflects the complete blockage of one or more coronary arteries.
The appearance of new left bundle branch block on the ECG in the same setting is also considered a STEMI. Once a STEMI is confirmed via the ECG, the race is on. The sooner the blood clot can be dissolved or removed, the more likely the patient will survive and experience less heart muscle damage.
STEMI treatment is a balance of time and technique. Clot-busting drugs or fibrinolytics that dissolve the clot can be administered intravenously in the field or at a medical facility, or may be given via the process of Percutaneous Coronary Intervention (PCI) at a specialty hospital. PCI involves inserting a long catheter into the femoral artery that is floated to the base of the aorta and then into the coronary arteries where the obstruction can be located with dye, the clot dissolved or removed and the narrow area dilated, and a stent or tube placed to keep the artery open.
Since PCI does offer additional interventions beyond clot lysis or removal, the current recommendation is to transport the STEMI patient to a PCI facility if the time from first medical contact in the field or in a medical facility to balloon opening (that means in the PCI suite, catheter in the artery) can be achieved in 90 minutes or less. If PCI within these parameters is not available, the current recommendation is to administer intravenous fibrinolytics within 30 minutes of first medical contact in the field or in a medical facility. Non-STEMI patients may undergo PCI at some time during their hospitalization, but are generally not as time-critical as the STEMI patient.
For EMS, it is clear that obtaining an ECG while providing care for the chest pain patient is critical to improving the quality of survival for STEMI patients through decreasing the time to clot intervention. EMTs at all levels should be allowed to obtain and transmit ECGs to their receiving facility. Advanced EMTs with additional training and demonstrated expertise should obtain and read ECGs and when appropriate administer fibrinolytics in the field under active medical oversight.
A system of care for the acute coronary syndromes can maximize patient outcomes in the same manner the injured patient benefits from a functional trauma system. EMS is an important evidence-based component within a cardiac care system and is essential for obtaining the highest degree of successful patient outcomes.
Recommended Reading: AHA STEMI Provider Manual
1. Kushner FG, Hand M, Smith SC Jr, King SB 3rd,Anderson JL, Antman EM, Bailey SR, Bates ER, Blankenship JC, Casey DE Jr, Green LA, Hochman JS, Jacobs AK, Krumholz HM, Morrison DA, Ornato JP, Pearle DL, Peterson ED, Sloan MA, Whitlow PL, Williams DO. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2009;54:2205–41.
2. Antman EM, Hand M, Armstrong PW, Bates ER, Green LA, Halasyamani LK, Hochman JS, Krumholz HM, Lamas GA, Mullany CJ, Pearle DL, Sloan MA, Smith SC Jr.
3. Kumar A, Cannon CP. Acute Coronary Syndromes: Diagnosis and Management, Part II. Mayo Clin Proc. 2009;84(11):1021-1036.
4. Sayad AJ, Roe, MT. The Role of Fibrinolytics in the Prehospital Treatment of ST-Elevation Myocardial Infarct (STEMI). J Emerg Med. 2008;34(4):405-416.
5. Zeymer U, Arntz HR, Dirks B, Ellinger K, Genzwurker H, Nibbe L, Tebbe U, Senges J, Schneider S. Reperfusion rate and inhospital mortality of patients with ST segment elevation myocardial infarction diagnosed already in the prehospital phase: Results of the German Prehospital Myocardial Infarction Registry (PREMIR). Resuscitation.2009;80:402-406.
6. Bata I, Armstrong PW, Travers A, Sookram S, Caine E, Christenson J, Welsh RC, WEST Study Group. Time from first medical contact to reperfusion in ST elevation myocardial infarction: a Which Early ST Elevation Myocardial Infarction Therapy (WEST) substudy. Can J Cardiol.2009;25(8):463-468.
7. Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE II, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction): developed in collaboration with the American College of Emergency Physicians, American College of Physicians, Society for Academic Emergency Medicine, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2007;50:e1–157.