EMT Acute Myocardial Infarction
There are many misconceptions regarding Acute Myocardial Infarctions, more commonly referred to as “heart attacks” by the layperson. Many who do not possess medical knowledge or have a limited background in medicine have misconceptions about what a heart attack truly is. This article will address this commonly misrepresented pathologic process and teach it at both a BLS and a basic ALS level as well as prepare you for MI/AMI based National Registry exam questions. While this article is “EMT acute myocardial infarction” adding elements of ALS protocol will allow you to have a projection of potential differences in care given, what to anticipate on a bridge unit (one in which an EMT-B has a paramedic partnet) or what care is given in a potentially upcoming career path if you decide to take your education to a Paramedic Level.
Acute MI is a subdivision of ACS (acute coronary syndrome), which is a parent term referring to a group of symptoms compatible with myocardial ischemia. This parent term contains STEMI, NSTEMI as well as unstable angina.
Broken down into its simplest form an Acute Myocardial Infarctions (MI) is just that, an Acute or sudden onset, Myocardial referring to the myocardium or central muscular layer of the heart, Infarction an obstruction of blood flow resulting in cellular death. This event most often results from the occlusion of a specific vessel, a coronary artery, which feed the heart muscle itself. These vessels branch off of the Ascending Aorta and project inferiorly providing circulation to the heart. An obstruction of one of these vessels results in myocardial (heart muscle) cell death to the area of the heart this vessel supplies, again due to lack of oxygen from a lack of blood supply. This phenomenon is also referred to as Ischemia, which is tissue death as a result of a lack of oxygen.
Causes of this ischemic attack include, but are not limited to, plaque rupture or spasm, coronary dissection, coronary embolus, arrhythmia, anemia or hypotension.
This occlusion is most often a result of long-term accumulation of plaque in the artery, often referred to as atherosclerosis. While the cause of the event may have accumulated over the duration of ones lifetime, these events are time sensitive, and cell death can result in as few as 20 minutes, again reinforcing the fact that these events are acute in nature.
Such cellular death can be permanent in nature, resulting in cardiac hypertrophy and fibrosis (stiffening). This byproduct can result in numerous short and long-term consequences, including but not limited to cardiac dysrhythmia, and heart failure due to altered ventricular compliance, and decreased contractility due to ventricular stiffness.
Signs and Symptoms
The National Registry Exam will often distinguish classic signs and symptoms, or male symptoms, from female, atypical, signs and symptoms of MI. Having male signs and symptoms referred to as classic is primarily a byproduct of men historically experiencing MI’s at a much higher rate than their female counterparts, but due to western lifestyle, and possible the increasing prevalence of females in the positions of high stress in the work force, levels of acute myocardial infarction are leveling out between the genders.
Classic symptoms include chest pain or pressure, which is often sub-sternal in origin and radiates to the arms, back and/or jaw. This patient will often appear with diaphoretic, pale skins, as well as nausea and vomiting. This patient may appear to be short of breath, have a heightened level of anxiety, and have the classic “impending feeling of doom.”
Female, atypical, signs of MI differ in that chest pain or pressure may not be the primary complaint. These patients may present with upper abdominal or epigastric pain, dizziness, or symptoms similar to that of a near-syncopal episode. Many signs and symptoms of panic attacks or anxiety can mimic that of an MI and only adding to this confusion is the atypical finding of Paresthesia or tingling in female MI patients. This tingling is found in toward the distal end of extremities and again can mimic a precursor to Carpopedal Spasms found in hyperventilation anxiety patients. While you may have a high index of suspicion for anxiety in many chest pain patients, always tread carefully with these patients and be thorough in your assessment regardless of personal biases or initial impressions. Don’t get burned by this.
Care and Treatment
BLS EMT Acute Myocardial Infarction Treatment
BLS level care includes frequent monitoring of vital signs, and supplemental oxygen if the patient has an O2 level of less than 94% or if they appear to be in respiratory distress but ventilation is adequate. Oxygen in this instance should be titrated to a patient’s comfort, but should not excessive and hyperoxygenation should be avoided If ventilation is not adequate and the patient appears to be in respiratory distress, begin assisted ventilation with the bag valve mask and high flow O2.
If this patient has their own prescribed Nitroglycerin tablets, administer, or assist in administering .4mg sublingual Nitro tablets or spray. This process can be repeated up to three times at a rate of q3-5 minutes. Always ensure that your patient has a systolic blood pressure of above 90mmHg prior to administering a dose of Nitro. If you are administering doses every 3 minutes, you should be taking a set of vitals every 3 minutes prior to your administration. Nitroglycerin is a relatively powerful vasodialator and can quickly result in a drop in a patient’s blood pressure. BLS providers can also often administer 324 mg ASA, or the dosage according to your local protocol.
If you are on a strictly BLS unit, strongly consider upgrading these patients for numerous reasons, IV access, 12 lead and continuous EKG monitoring and medication administration being only a few.
ALS/EMT-P Acute Myocardial Infarction Treatment
The most prominent difference in initial EMS care provided by ALS staff is the presence of a 12 lead EKG. BLS care providers can get a routine set of vital signs, and assess signs and symptoms, but an EKG is the most definitive pre-hospital diagnostic test available to EMS staff for Acute Myocardial Infarctions. While ALS providers do not possess the capacity (currently) to run in the field labs, and obtain a troponin, the presence of a 12 lead EKG with ST Elevation in multiple contiguous leads with reciprocal changes can strongly add to your index of suspicion of acute MI.
While BLS level providers can administer a patients own SL Nitro up to 1.2mg, ALS providers are recommended to apply 1 inch of transdermal Nitro paste, again give 324 mg (or your local protocols recommended dose) ASA, and .4mg SL Nitro every 3-5 minutes. IV access is strongly recommended due to patient’s tendency have a decrease in blood pressure due to vasodilation or code during these events.
Again oxygen administration should match the level of patients dyspnea, with BVM assisted ventilation for patients who are not adequately ventilating, and oxygen titrated to keep a patients o2 over 94% without hyperoxygenating.
Morphine for pain management is part of our local protocol, but variances from region to region exist. As always, refer to your local protocol guide and do not operate out of your scope of practice.
Long Term Care
While these patients may show slight improvement en route due to systemic vasodilation, ASA effects, pain management, and O2 supplementation, the end goal is early determination of MI, and transport to an appropriate cardiac facility. Once the facility has confirmed the MI the patient can expect cardiac catheterization followed by surgical interventions including a coronary artery bypass graft (CABG), or a percutaneous coronary intervention. Medical reperfusion techniques are also commonly used as is fibrinolytic therapy.