Myocardial Infarction (MI)

WHAT WENT WRONG?

Blood supply to the myocardium is interrupted for a prolonged time due to the blockage

of coronary arteries. This results in insufficient oxygen reaching cardiac muscle,

causing cardiac muscles to die (necrosis). MI is commonly known as a heart attack.

The area of infarction is often due to build-up of plaque over time (atherosclerosis).

It may also be due to a clot that develops in association with the atherosclerosis

within the vessel. Patients are typically (not always) symptomatic, but some

patients will not be aware of the event; they will have what is called a silent MI.

 PROGNOSIS

The outcome depends on the coronary artery that is affected. The earlier the person

enters the healthcare system, the better the prognosis is, because emergency

measures will be available for otherwise fatal arrhythmias. There is a better outcome for patients who receive adequate medical attention

and make appropriate lifestyle changes post-myocardial infarction. Cardiac rehabilitation

can help patients make these changes safely.

HALLMARK SIGNS AND SYMPTOMS

• Chest pain that is unrelieved by rest or nitroglycerin, unlike angina

• Pain that radiates to arms, jaw, back and/or neck

• Shortness of breath, especially in the elderly or women

• Nausea or vomiting possible

• Maybe asymptomatic, known as a silent MI, which is more common in diabetic

patients

• Heart rate >100 (tachycardia) because of sympathetic stimulation, pain, or

low cardiac output

• Variable blood pressure

• Anxiety

• Restlessness

• Feeling of impending doom

• Pale, cool, clammy skin; sweating (diaphoresis)

• Sudden death due to arrhythmia usually occurs within first hour

INTERPRETING TEST RESULTS

• EKG.

• T-wave inversion—sign of ischemia.

• ST-segment elevated or depressed—sign of injury.

• Significant Q-waves—sign of infarction.

• Decreased pulse pressure because of diminished cardiac output.

• Increased white blood count (WBC) due to inflammatory response to injury.

• Blood chemistry:

• Elevated creatine kinase MB (CK-MB)—usually done serially, the numbers

will rise along a predetermined curve to signify myocardial damage

and resolution.

• Elevated troponin I- and troponin T-proteins elevated within one hour of

myocardial damage.

• Less than 25 ml/hr of urine output due to lack of renal blood flow.

TREATMENT

Treatment is focused on reversing and preventing further damage to the myocardium.

Early intervention is needed to have the best possible outcome. Thrombolytic

therapy is instrumental in reducing mortality. A three-hour time window is

ideal for maximizing benefit. Medications are used to enhance blood flow to the

heart muscle while reducing the workload of the heart. Supplemental oxygen is

used to help meet myocardial oxygen demand. Data from coronary angioplasty

and percutaneous coronary intervention (stenting) of an occluded artery have been

impressive. Following the acute management, the patient will have to make lifestyle

changes—altering diet and exercise, stopping smoking, and so on.

• Administer oxygen, aspirin.

• Administer antiarrhythmics because arrhythmias are common as are conduction

disturbances.

• Amiodarone.

• Lidocaine.

• Procainamide.

• Electrical cardioversion for unstable ventricular tachycardia. In cardioversion,

an initial shock is administered to the heart to re-establish sinus rhythm.

• Administer antihypertensive to keep blood pressure low.

• Hydralazine.

• Percutaneous revascularization.

• Administer thrombolytic therapy within 3 to 12 hours of onset because it can

re-establish blood flow in an occluded artery, reduce mortality, and halt the

size of the infarction.

• Alteplase.

• Streptokinase.

• Anistreplase.

• Reteplase.

• Heparin following thrombolytic therapy.

• Administer calcium channel blockers as they appear to prevent reinfarction

and ischemia, only in non–Q-wave infarctions.

• Verapamil.

• Diltiazem.

• Administer beta-adrenergic blockers because they reduce the duration of ischemic

pain and the incidence of ventricular fibrillation; decreases mortality. • Propranolol.

• Nadolol.

• Metroprolol.

• Administer analgesics to relieve pain, reduce pulmonary congestion, and decrease

myocardial oxygen consumption.

• Morphine.

• Administer nitrates to reduce ischemic pain by dilation of blood vessels; helps

to lower BP.

• Nitroglycerin.

• Place patient on bed rest in CCU.

• No bathroom privileges. Bedside commode only.

• Low-fat, low-caloric, low-cholesterol diet.

DIAGNOSES

• Ineffective tissue perfusion

• Decreased cardiac output

INTERVENTION

• Monitor:

• Cardiovascular—look for changes or instability in pulse, heart sounds,

murmur.

• Respiration—look for changes, fluid in lung fields, shortness of breath.

• EKG during attack—12-lead during any episode of pain.

• EKG continuous monitoring for arrhythmias.

• Vital signs—check for changes in BP, pulse quality, peripheral pulses.

• Pulse-oximetry monitoring.

• Explain to the patient:

• Change to a low-fat, low-cholesterol, low-sodium diet.

• The difference between angina pain and myocardial infarction pain.

• When to take nitroglycerin.

• Medication.

• Smoking cessation.

• Limit activities.

• Need for cardiac rehabilitation.

• Stress reduction.

• Lifestyle changes such as increase in exercise, diet changes.

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