According to the chest pain guidelines the faster the diagnosis can be made and the occlusion reversed, the more likely the patient is to salvage myocardial tissue and benefit from improved outcomes.
Cardiovascular disease is a dominant cause of morbidity and mortality in the United States and acute myocardial infarction (MI) is one of the major underlying etiologies.
Acute MI is a medical emergency that is precipitated when coronary occlusion leads to ischemia and then necrosis of cardiac myocytes.
The necrosis will often precipitate a cardiac arrhythmia (e.g., ventricular fibrillation), which is a major cause of death for patients presenting in the acute phase.
The diagnosis of an acute MI is based on the patient’s history and diagnostic testing, including an electrocardiogram (ECG) and serum enzymes.
In nondiabetic patients, the major symptom of acute MI is pain. This pain is usually described as severe. It is located in a retrosternal area and may radiate to either the arms or neck.
The characteristic quality of the pain is described as pressurelike or bandlike; however, other descriptions including burning, aching, and crushing have also been used.
The pain usually lasts beyond 20 to 30 minutes and does not dissipate. Associated symptoms include nausea, vomiting, shortness of breath, dizziness, and diaphoresis.
In the setting of a possible acute MI, the ECG is a readily available, noninvasive, easy-to-obtain diagnostic test that has excellent sensitivity and specificity. The ECG provides information on the distribution of changes and the impact on cardiac rhythm.
The pattern of ST-segment elevation representing a current of injury is usually associated with acute MI and implies a coronary occlusion. This is helpful for triaging for strategies of reperfusion according to chest pain guidelines.
In addition to the ECG, cardiac enzymes are particularly sensitive for detecting myocardial damage. These proteins are released from the myocardial cells that have sustained damage. Troponins are particularly important for the diagnosis of acute MI since under normal conditions, they are not found in the serum.
These enzymes first become detectable from 2 to 4 hours after injury and persist for days. Creatine kinase (CK) and the MB subtype have for many years dominated the clinical arena as the major cardiac marker in the setting of acute MI now being supplanted by troponins.
These tests are important early markers of myocardial necrosis but take longer to be detected and disappear from the serum more rapidly than troponins. It must be noted that in postoperative patients, creatine phosphokinase (CPK) and troponin have not been shown to be as sensitive markers for cardiac damage as they are in nonsurgical patients.
What are chest pain guidelines
The management of patients presenting with chest pain guidelines of acute MI should trigger a number of immediate events. The longest delay in therapy is usually related to the patient’s delay in seeking care. Denial of the pain and the hope that it will go away are important underlying reasons for this phenomenon.
When the patient presents to the emergency department with this symptom the chest pain guidelines consist of, a focused history, physical examination, and electrocardiogram should be obtained.
If the appropriate clinical symptoms and ECG findings suggest an acute MI, aggressive management should include intravenous access, oxygen, sublingual nitroglycerin, morphine, and beta-blocker therapy. If the patient presents within 12 hours of symptoms, aggressive methods to achieve reperfusion should be considered.
The recommended strategy in chest pain guidelines for achieving reperfusion is cardiac catheterization with angioplasty if the institution is capable of achieving a door-to-balloon time of <90 minutes.
This strategy in chest pain guidelines begins with the administration of glycoprotein IIb/IIIa inhibitors in addition to the more generic therapies described previously.
This strategy has the advantage of achieving higher recanalization rates, reducing residual stenosis, and improving the outcomes in the setting of cardiogenic shock. When an institution is unable to provide primary angioplasty strategies, thrombolytic therapy can be attempted.
A number of contraindications to thrombolytic therapy need to be considered before providing this intervention and include bleeding, a history of stroke, severe hypertension, recent trauma or surgery, pregnancy, aortic dissection, and intracranial or spinal cord neoplasms.