Myocardial infarction management
Myocardial infarction management involves salvaging as much myocardium as possible and to prevent further complications, thus the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin are usually administered as soon as possible. Morphine was classically used if nitroglycerin was not effective however it may increase mortality in the setting of NSTEMI. A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use.
Aspirin is useful not only for the primary prevention of vascular events but is also effective across the entire spectrum of acute coronary syndromes and forms part of the initial management strategy for patients with suspected STEMI. Aspirin has been shown to markedly reduce mortality and thus should be taken as soon as possible in those without an allergy to it. Aspirin has an antiplatelet effect which inhibits formation of further thrombi (blood clots) that clog arteries. Chewing is the preferred method of administration, so that it can be absorbed quickly. Dissolved soluble preparations or sublingual administration can also be used. Because low doses take several days to achieve full antiplatelet effect, U.S. guidelines recommend a dose of 162–325 mg. Australian guidelines recommend a dose of 150–300 mg. Additionally, the antiplatelet agent clopidogrel improves outcomes in those who will be conservatively managed or undergo percutaneous coronary intervention. It however may worsen outcomes in those who need urgent coronary artery bypass surgery.
Nitroglycerin is used in the treatment of ACS/IHD to relieve anginal symptoms. It is associated with the decrease in myocardial stress due to peripheral vasodilation. The decrease of stress also decreases oxygen demand of the heart. The first line treatment for symptomatic relief of angina is sub-lingual nitroglycerin. Other formulations such as spray and IV can also be used. In the body nitroglycerin donates three nitric oxide molecules, which activate a second messenger system leading to release of calcium ions. The release of calcium ions leads to a relaxation of vascular smooth muscles and vasodilation. Nitroglycerin should not be given if any phosphodiesterase type 5 inhibitors such as Viagra, Cialis, Stondra, and Levitra have been taken by the casualty within the previous 24–48 hours as the combination of the two could cause a serious drop in blood pressure. It should not be given to patients with systolic blood pressure (SBP) less than 90mmHg or 30mmHg or more below baseline.
In theory β-blockers decrease the effect of the sympathetic nervous system on the heart. Since it is known that the sympathetic nervous system increases the heart rate and blood pressure in order to increase the cardiac output. Hence its blockage spares the heart the extra work load. So, the immediate intravenous administration of beta blockers reduces cardiac index, heart rate and blood pressure. Favorable effects are reduction in chest pain, in the proportion of patients with threatened infarction who actually evolve STEMI and in the development of ventricular arrhythmias. It is reasonable to administer iv beta blockers promptly to STEMI patients, especially if a tachyarrhythmia or hypertension is present, in the absence of signs of heart failure or low output, increased risk of developing shock or other relative contraindications to beta blockers.
Some new data showed that early treatment of heart attack patients with an inexpensive beta-blocker drug called metoprolol, while in transit to the hospital, can significantly reduce damage to the heart during a myocardial infarction Inpatient beta-blocker use can be coupled with transvenous pacing, where a temporary pacemaker allows for the benefits of beta-blocker therapy while preventing uncontrolled bradycardia and maintaining sufficient cardiac output.
Myocardial Energy Metabolism Regulator
Mildronate is a clinically used pharmacological preconditioning agent and anti-ischemic drug. It acts as a myocardial energy metabolism regulator by inhibiting fatty acid oxidation, and the carnitine biosynthesis and transport pathways, in particular gamma-butyrobetaine dioxygenase and carnitine acetyltransferase. By regulating the effective carnitine concentration, treatment with mildronate shifts the myocardial energy metabolism from fatty acid oxidation to the more favourable glucose oxidation under ischemic conditions.
The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era. Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery.
Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with antiplatelet drugs and anticoagulated. If their condition remains (hemodynamically) stable, they can be offered either late coronary angiography with subsequent restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however.
The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding.
At least 10% of patients with STEMI do not develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted.
Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents. Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial infarction.
Cardiac rehabilitation aims to optimize function and quality of life in those afflicted with a heart disease. This can be with the help of a physician, or in the form of a cardiac rehabilitation program.
Physical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, stress and mood. Some patients become afraid of exercising because it might trigger another infarct. Patients are stimulated to exercise, and should only avoid certain exerting activities. Local authorities may place limitations on driving motorised vehicles. In most cases, the advice is a gradual increase in physical exercise during about 6–8 weeks following an MI. If it doesn't feel too hard for the patient, the advice about exercise is then the same as applies to anyone else to gain health benefits, that is, at least 20–30 minutes of moderate exercise on most days (at least five days per week) to the extent of getting slightly short of breath.
When symptoms of myocardial infarction occur, people wait an average of three hours, instead of doing what is recommended: calling for help immediately. Acting immediately by calling the emergency services can improve outcomes for two reasons. First and most importantly, the emergency services can immediately save life from ventricular fibrillation, most often primary ventricular fibrillation, which occurs unexpectedly in more than 10% of all infarctions especially during the first hour of symptoms and second, immediate treatment of myocardial infarction can prevent sustained damage to the heart ("time is muscle").
Emergency Medical Services (EMS) Systems vary considerably in their ability to evaluate and treat patients with suspected acute myocardial infarction. Some provide as little as first aid and early defibrillation. Others employ highly trained paramedics with sophisticated technology and advanced protocols. Paramedic services are capable of providing oxygen, IV access, sublingual nitroglycerine, morphine, and aspirin. Some advanced paramedic systems can also perform 12-lead ECGs. If a STEMI is recognized the paramedic may be able to contact the local PCI hospital and alert the emergency room physician, and staff of the suspected AMI. Some Paramedic services are capable of providing thrombolytic therapy in the prehospital setting, allowing reperfusion of the myocardium.
With primary PCI emerging as the preferred therapy for ST-segment elevation myocardial infarction, EMS can play a key role in reducing door-to-balloon intervals (the time from presentation to a hospital ER to the restoration of coronary artery blood flow) by performing a 12-lead ECG in the field and using this information to triage the patient to the most appropriate medical facility. In addition, the 12-lead ECG can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to the arrival of the patient. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel in areas where the cardiac cath lab is not staffed 24 hours a day. Even in the absence of a formal alerting program, prehospital 12-lead ECGs are independently associated with reduced door to treatment intervals in the emergency department.
Cocaine associated myocardial infarction should be managed in a manner similar to other patients with acute coronary syndrome except beta blockers should not be used and benzodiazepines should be administered early. The treatment itself may have complications. If attempts to restore the blood flow are initiated after a critical period of only a few hours, the result may be a reperfusion injury instead of amelioration.
In wilderness first aid, a possible heart attack justifies evacuation by the fastest available means, often meaning the initiation of a MEDEVAC. The suspicion or provisional diagnosis of an MI means that it is inappropriate for the patient to walk out of the wilderness setting and will require them to be carried or conveyed in a vehicle. Aspirin, nitroglycerin, and oxygen can all be given with relative ease in a wilderness setting and should be administered as soon as possible in suspected cases of MI. Wilderness management of cardiac arrest differs slightly from that carried out in an urban setting in that it is generally considered acceptable to terminate a resuscitation attempt after 30 minutes if there has been no change in the patient's condition.
Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using the on-board first aid kit, which may contain some cardiac drugs (such as glyceryl trinitrate spray, aspirin, or opioid painkillers), an AED, and oxygen. Pilots may divert the flight to land at a nearby airport. Cardiac monitors are being introduced by some airlines, and they can be used by both on-board and ground-based physicians.
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