Myocardial infraction (MI) causes the death of myocardial tissue from inadequate blood supply to the myocardium.
MIs are classified according to the layer of myocardial tissue involved.
A subendocardial or nontransmural MI is limited to the inner half of the ventricular muscles; a transmural MI involves the entire thickness of the myocardium.
An anterior MI usually involves occlusion of the left anterior descending coronary artery.
An inferior or diaphragmatic MI usually involves occlusion of the right coronary artery.
A posterior MI involves occlusion of the right coronary artery or circumflex branch of the left coronary artery and usually also involves the lateral or inferior wall of the left ventricle.
A lateral MI is relatively rare, with damage confined to the lateral wall, although it may occur in combination with an anterior MI.
Right ventricular infraction occurs when occlusion of the right coronary artery damages the right ventricle; it occurs most often with an inferior MI.
An anterior or lateral MI produces significantly higher mortality, more damage to the myocardium, more conduction disturbances, and increased occurrences of congestive heart failure and cardiogenic shock than does an inferior or posterior MI.
Complications of Myocardial Infarction includes dysrhythmias, cardiogenic shock, thromboembolism, pericarditis, rupture of the myocardium, ventricular aneurysm, congestive heart failure.
Occlusion of coronary artery blood flow from coronary thrombus over a high-grade lesion
Coronary artery vasospasm
Increased oxygen demands
Decreased coronary artery perfusion pressure
C. Assessment Findings
Chest pain (typically chest pain is persistent and crushing; located substernally with radiation to the arm, neck, jaw or back; and unrelieved by rest or nitrates. A silent MI may produce no pain.)
Diaphoresis and cool, clammy and pale skin.
Nausea and vomiting.
Dyspnea with or without crackles.
Palpitations or syncope.
Restlessness and anxiety or feeling of impending doom.
Tachycardia or bradycardia.
Decreased blood pressure.
Altered S3 heart sound (indicates left ventricular failure)
D. Diagnostic Test Findings
Serum creatine phosphokinase (CPK-MB isoenzyme elevation greater than established institutional criterion that begins 4 to 8 hours after infraction, peaks at 24 hours, and lasts for 72 hours after infraction.
Serum lactate dehydrogenase (LDH); LDH1 greater than DH2; this isoenzyme pattern of elevation develops 12 to 24 hours after infraction, peaks at 36 to 72 hours, and returns to normal within 10 days of the infraction.
ECG: changes in leads over area of infract: ST segment elevation (indicating injury to myocardial tissue), ST segment depression (in leads that view the opposite wall), T-wave flattening and inversion (indicating ischemia of the myocardial tissue), and Q-wave abnormalities (representing tissue death), which are clinically significant if the Q wave is greater than one third of the total QRS height or more than 0.04 second wide.
Chest X-ray: cardiac enlargement and signs of left ventricular failure (pulmonary congestion); may also be normal.
Echocardiogram: abnormalities of left ventricular wall motion and valve competency.
Hemodynamic monitoring: increased pulmonary artery pressure (PAP), increased PAWP, decreased cardiac output, and increased SVR, depending on extent of the MI.
E. Patient Care Management Goal: To relieve acute pain, reduce the cardiac work load, prevent and treat arrhythmias, and manage fluid imbalances and limit infract size by reperfusion
Administer oxygen to relieve ischemia at a flow rate based on institutional policy and the patient’s condition.
Assess and document characteristics of pain: location, duration, intensity (have patient grade pain on a scale from 1 to 10), precipitating factors, relief measures, and associated symptoms.
Assess and document continuous ECG rhythm, vital signs, mental status, heart and lung sounds, urine output, and any signs or symptoms indicating changes in these parameters.
Assess vital signs with symptoms of chest pain, and compare to baseline.
Begin I.V. nitroglycerin titrated until acute pain is relieved; check blood pressure every 15 minutes or according to institutional policy; and maintain systolic blood pressure greater than 90 mm Hg or according to institutional protocol; document the patient’s response to therapy.
Administer I.V. morphine in small doses to relieve pain, to reduce anxiety, and to decrease preload and myocardial oxygen consumption.
Consider antiarrhythmic I.V. drug therapy prophylactically or as ordered, based on institutional policy; lidocaine is the drug of choice based on the American Heart Association’s advanced cardiac life support protocol.
Administer thrombolytic therapy with tissue plasminogen activator or streptokinase within the first few hours to lyse the clot after any chest pain suggesting an infarction.
Keep in mind that the doctor may order anticoagulants to prevent clot formation.
If a pulmonary artery catheter is in place, assess and document PAP, PAWP, cardiac output, and SVR, as ordered.
Run a 12-lead ECG when pain occurs and then daily for 3 days to evaluate any evolutionary changes associated with MI.
Monitor serum potassium levels, and report outside normal limits; potassium levels should be kept higher than 4.0 mEq/liter to reduce the risk arrhythmias.
Enforce activity restrictions to decrease oxygen requirements.
Maintain accurate intake and output records and daily weights to assess fluid status.
Begin the patient on a low-cholesterol, low-sodium diet to alter modifiable risk factors.
Consider PTCA to improve blood flow through the stenotic coronary arteries.
Remember that a CABG may be indicated when medical treatment has been unsuccessful, based on the patient’s symptoms and the cardiac catheterization report.
Provide patient education, and ensure that the patient can recognize signs and symptoms necessitating medical attention (i.e., unrelieved chest pain after taking three nitroglycerin tablets sublingually 5 minutes apart) and understands guidelines for resuming sexual activity after discharge.
Work with the patient and family to identify the patient’s risk factors and necessary life-style modifications (smoking cessation, stress management, diet modification).
Refer the family to appropriate sources for CPR training.
Ensure that the family can activate the emergency medical system if problems occurs at home.