NURSING CARE OF CLIENTS

An acute myocardial infarction (MI), necrotis (death) of cell in an area of cardiac muscle.
If circulation to the affected cardiac muscle is not restored in a timely manner, loss of functional myocardium affects the heart’s ability to maintain an effetive cardiac output and may ultimately result in cardiogenic shock and death.
MI usually follows the sudden occlusion of a coronary flow to the heart muscle.

Because the heart muscle must function continuously, blockage of blood to the muscle and the development of necrotic areas within the myocardium represent a serious event

Angina as a result of ischemia causes reversible cellular injury, and infarction is the result of sustained ischemia, causing irreversible cellular death.

Risk factors and incidence :
US : Every year approximately 1.500.000 fall victom to heart attacks.. MI is the leading cause of deaths each year. Most deaths occur within the first 2 hours after the onset of symptom. Approximately 45 per cent of all heart attack clients are under the age of 65 years, and 5 per cent are under the age of 40 years(Polaski & Tatro, 1996).

The most common cause of MI is complete or nearly complete occlusion of a coronary artery due to ongoing atherosclerosis.

The vessel lumen slowly occludes and is often blocked with a thrombus.

Risk factor for MI : Age, gender, heredity, race, smoking, obesity, hyperlipidemia, hypertension, diabetes, stress, sedentary life-style, and personality type.

Phatophysiology
MI occur when a coronary artery becomes critically occluded, blocking blood flow to a portion of cardiac muscle for a prolonged period of time.
Usually caused by a thrombus (clot) developing at a site of arterial narrowing.
May also by ulceration and rupture of atherosclerotic plaquestimulates platelet aggregationplatelet-thrombus formationclot formthe vessel becomes occluded.

Cellular injury  inadequate oxygen and nutrients.
More than 20 to 45 minutes irreversible hypoxemic damage-cellular death and tissue necrosis-intracellular enzymes are released through damaged cell membranes into interstitial spaces  serum enzimes is elevated (CK-MB, LDH).

Infarctions are described by the area of occurrence as anterior, inferior, lateral, or posterior wall infartions. Common combinations of are the anterolateral or anteroseptal MI. An inferior MI is also called a diaphragmatic MI
Clinical Manifestations
•Cardinal symptom of MI is chest pain.
•The pain may radiate to the neck, jaw, shoulder, back, or left arm. Also, the pain may present near the epigastrium.
•Nausea anmd vomiting :Nausea and vomiting can result from reflex stimulation of the vomiting centre by the serve pain.
•Sympathetic nervous system stimulation :Inreased catecholamines are released. Increased symphatetic nervous system stimulation results in diaphoresis and vasoconstriction of peripheral blood vessels.
•Fever :The temperature may increase within the first 24 hours up to 38C  systemic manifesttion of the imflamatory process caused by cell death in the infarcted myocardium.
•BP and HR : BP and HR mey be elevated. Later BP may drop because of decreased CO.
•Urine output may be decreased.
•Cracles may be noted in the lungpersisting for several hours to several days.
Complications :
1.ArrhythmiasMost common complications.
Arrhythmias are caused by any condotion that affects the myocardial cell sensitivity to nerve impulses, such a ischemia, electrolyte imbalances, an sympathetic nervous system stimulation.
2.Congestive heart failure : when the pumping power of the heart has diminished.
AMIcommon of LV dysfungction in the first 24 hours
3.Cardiogenic shock  when inadequate oxygen and nutriens are supplied to the tissues because of severe LV failure.
4.Ventricular aneurysm : Result when the infarcted myocardial wall becomes thinned and bulges out during contraction.
5.Pericarditis : Inflammation of the visceral or parietal pericardium, or both cardiac compressiondecreased ventricular filling and emptyingcardiac failure.

tiar@2007