Acute MI interventions

Acute MI is one condition in a spectrum of illnesses known as acute coronary syndrome. The cause of acute MI can be traced to several causes, but the main perpetrator of a "heart attack" is coronary artery disease (CAD). Acute MI is an emergency diagnosis that requires quick thinking on the part of the nurse and immediate intervention from the nurse as well as the physician and other healthcare staff. The majority of MI-associated deaths are a result of fatal arrhythmias, such as ventricular fibrillation, that can be stopped with prompt intervention, including emergency cardiopulmonary resuscitation (CPR), defibrillation, and advanced cardiac life support (ACLS).

Treatments for acute MI are ever changing and have resulted in a decrease in MI-related mortality in the past decades. Thrombolytic therapy, a revolutionary treatment a few years ago, has been replaced with percutaneous coronary intervention (PCI) as the gold standard for care because of its proven effectiveness in treating acute MI.

The heart is a muscular pump responsible for circulating oxygenated blood to all cells in the body and returning deoxygenated blood to the lungs. To perform effectively, the myocardium is in constant need of an oxygen supply, which is provided by two main coronary arteries and their branches:

Left main coronary artery (LMCA)–supplies blood to the chambers on the left side of the heart through its branches, the left anterior descending (LAD) artery and the circumflex (Cx) artery. The LAD provides blood to the front of the left side of the heart. The circumflex (or "circ") circles the heart to supply blood to the side and posterior portions of the heart.

Right coronary artery (RCA)–supplies blood to the right side of the heart, including the sinoatrial (SA) node and the atrioventricular (AV) node. These nodes, particularly the SA node, work to regulate the heart's rate.

When the blood supply to the heart is compromised for more than 20 minutes, irreversible tissue damage and necrosis occur, that is, a myocardial infarction. Although any condition that disrupts blood flow to the heart can cause tissue damage, atherosclerosis is the most common cause. Atherosclerosis is the buildup of fatty deposits or plaque in the walls of the arteries. The plaque in the arteries can break through the endothelium and come in contact with blood flow. The rough surface of the plaque activates the body's clotting mechanisms, and a thrombus forms. The thrombus, or clot, occludes the vessel and prevents blood flow to the portion of the myocardium supplied by that vessel. Lack of blood flow means lack of oxygen and tissue damage occurs.

Healthcare providers classify MI as a non-ST-segment elevation MI (NSTEMI or non-STEMI) or a STEMI.

STEMI–complete occlusion of a coronary vessel characterized by elevation of the ST segment in certain leads on a 12-lead EKG (see section on 12-lead EKG interpretation for details about specific diagnostics) and positive cardiac enzymes.

NSTEMI–incomplete occlusion of a coronary vessel and no ST-segment elevation on a 12-lead EKG; however, cardiac enzymes are positive.

The severity of MI depends on several factors: the amount of occlusion, the length of time blood supply is compromised, and whether the patient has collateral circulation to the area supplied by the occluded vessel.

Signs and Symptoms of Acute MI

Unfortunately, the majority of patients who experience an acute MI do so outside the hospital, such as at home or in the community, and away from immediate medical care. Some research has shown that most patients do not seek medical care for 2 hours or more after the onset of symptoms, and a fairly large number of people wait 12 or more hours. Reasons for delay may include patients' failure to recognize the seriousness of the problem; denial of symptoms or attributing symptoms to other illnesses, such as heartburn or anxiety; and limited access to a healthcare facility.

People can have difficulty recognizing the symptoms of MI because they can vary by individual. For example, men suffering from acute MI more commonly complain of chest pain, whereas women may complain of pain between their scapulae. The most common and cardinal symptom of an acute MI is chest pain, and some people, such as people with diabetic neuropathy and the elderly, may suffer no symptoms, a condition called silent MI.

Despite the variance in symptoms, MI presents with a few "classic" symptoms:

Chest pain is described as squeezing or pressure in the area of the sternum (the patient may describe the pain as "an elephant sitting on my chest"). The pain lasts longer than 30 minutes, and rest, nitroglycerin, and a change in posture or position do not resolve the pain.

The pain radiates to the neck, jaw, shoulder, arms, or back.

In addition to pain, the patient experiences dyspnea, diaphoresis, nausea, or vomiting. Some patients may complain of discomfort that feels like "heartburn."

Syncope or near syncope that cannot be attributed to any other condition.

Feeling of impending doom.

It is important to note that some patients will experience all of these symptoms; others may experience only one or a few. Contrary to what many people believe, symptom onset occurs most frequently at rest and in the early hours of the morning.

Complications Associated With Myocardial Infarction:

Amazing advances have been made in the treatment of acute MI over the past several years; however, it is still one of the leading causes of death. This is due to the serious complications usually associated with an infarction. These include coronary artery reocclusion, heart failure and cardiogenic shock, and arrhythmias. Nurses play an important role in assessing the patient for signs and symptoms of complications and assisting with early intervention.

  • Coronary Artery Reocclusion: A small number of patients will experience reocclusion of the artery after thrombolytic therapy even when preventative measures are taken. This happens because, although, the clot in the artery has been dissolved, the athersclerotic plaque is still present and if anticoagulation is inadequate, another thrombus may form. About 50% of the reocclusions occur within the first 24 hours following thrombolytic therapy. Symptoms such as chest pain, nausea, diaphoresis, and ST segment elevation will usually be similar to those experienced with the original MI. With this in mind, it is crucial to monitor the patient closely and be aware of changes indicative of reocclusion. Since readministration of a thrombolytic agent is not recommended, the patient will need to have a PTCA or CABG if angioplasty is not an option or unsuccessful.
  • Heart Failure and Cardiogenic Shock: Congestive heart failure following a myocardial infarction can range from mild to severe, depending on the extent of ventricular damage. Heart failure occurs when myocardial tissue is damaged and the ventricle no longer works as an efficient pump. In right-sided failure, the compromised right ventricle causes fluid to back up in the peripheral circulation; in left-sided heart failure, fluid backs up in the pulmonary circulation. Signs of heart failure, including shortness of breath; hypoxia; production of pink, frothy sputum; hypotension; oliguria; confusion or changes in level of consciousness; and tachycardia.
    Patients with heart failure can rapidly decline into cardiogenic shock. Cardiogenic shock occurs when 40% or more of the myocardium has been affected by the infarction. Because the heart is incapable of contracting with sufficient force to pump enough blood, the vital organs and peripheral tissues cease to function as a result of ischemia. The patient may experience the following symptoms: pulmonary congestion, diaphoresis, cool extremities, and mental confusion. Treatment for cardiogenic shock is aggressive and can include fluid replacement, inotropic drugs, and an intra-aortic balloon pump (an invasive device used to decrease ventricular workload and improve coronary artery perfusion).
    Unfortunately, death occurs in about 85% of patients who develop cardiogenic shock.
  • Arrhythmias: Successful thrombolysis can cause a variety of cardiac arrhythmias, such as ventricular tachycardia, premature ventricular contractions, accelerated idioventricular rhythm, and sinus bradycardia. These are generally accepted as normal consequences of coronary reperfusion, and treatment is not necessary unless the patient becomes unstable.

Ventricular fibrillation. The majority of sudden cardiac deaths are because of ventricular fibrillation, or v fib. This arrhythmia results in an ineffective quivering of the ventricles and no cardiac output. Treatment includes basic life support (airway, breathing, and circulation), defibrillation, and advanced cardiac life support. The sooner the ventricular fibrillation is treated, the greater the chance of survival for the patient.

Ventricular tachycardia. Patients who have suffered an acute MI may experience ventricular tachycardia, or v tach. This ventricular arrhythmia can be benign or it can be life threatening. Patients may be asymptomatic or they may experience shortness of breath, chest discomfort, palpitations, and syncope. Patients may be given an antiarrhythmic, such as lidocaine, procainamide, or amiodarone, to reestablish sinus rhythm. If the patient is unstable, electrical cardioversion may be conducted in an attempt to convert the myocardium to a sinus rhythm. This arrhythmia is most common in patients who have experienced an anterior or anterolateral MI.

Sinus bradycardia and heart block. Bradycardia is a slowing of the heart rhythm. The patient may experience hypotension and syncope which usually responds to oxygen and atropine. Heart blocks occur as a result of problems in the atrioventricular (AV) node of the conduction system. Electrical impulses are not conducted from the atrium to the ventricles, which can cause a decrease in cardiac output. To correct the arrhythmia, patients may need transcutaneous (external) pacing or surgery to insert a transvenous (internal, temporary) pacemaker.

Diagnosis of Acute MI

Although prolonged chest pain, dyspnea, and diaphoresis are considered the classic symptoms of an acute MI, they can be associated with other disease processes as well. Also, not every patient with chest pain is experiencing an acute MI. Therefore, along with a thorough physical examination and chest x-ray, evidence-based practice dictates healthcare professionals to obtain a 12-lead EKG and cardiac enzymes as soon as the patient reports symptoms.

12-Lead EKG InterpretationThe 12-lead EKG is a tool used to record the electrical activity of the heart. The EKG is a reliable way to determine whether a patient is suffering an acute MI and whether it is a STEMI or non-STEMI. All patients suspected of having an acute MI should be given a 12-lead EK within 10 minutes of arrival to the hospital or, if the patient is already admitted, when symptoms of MI first present. Because of the evolving process of acute MI, it may be necessary to take several recordings as the patient experiences changes in symptoms.EKGs provide much information about a patient's cardiac status, and interpreting them can be quite complicated.