MYOCARDIAL INFARCTION
Myocardial Infarction refers to the process by which myocardial tissue is destroyed in regions of the heart that are deprived of an adequate blood supply because of a reduced coronary blood flow.
Causes
Atherosclerosis narrowing of a coronary artery
Embolus/Thrombus complete occlusion of an artery.
Shock and haemorrhage decreased coronary blood flow.
Pathophysiology
Etiological factors.
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Decreased blood supply to the myocardial area
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Decreased oxygen supply to the myocardial tissue.
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Cell necrosis.
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Area - becomes soft and then eventually fills in with firm, fibrous scar tissue
Survival and extent of restrictions depend upon the amount of myocardial damage and the area of the heart affected. Death may occur immediately or within a few hours. Obviously, the remaining viable heart tissue must compensate for the loss of functional tissue.
Types of Myocardial Infarction
1. Anterior wall infarction: The anterior wall of the left ventricular is infarcted due to an occlusion of the left anterior descending artery,
Anteroseptal infarction: The papillary muscles of the left ventricular and the intraventricular septum may be involved.
2. Lateral wall infarction. Results from occlusion of the lateral branch of the left circumflex artery.
Anterolateral obstructed. Anterior descending and the left circumflex branches are
3. Inferior wall infarction: The part of the left ventricular which rests on the diaphragm is affected due to occlusion of the right coronary artery.
4. Posterior wall infarction: Due to occlusion of the posterior branch of either the right coronary or left circumflex artery.
5. Right ventricular infarction: The right ventricular may infarct in conjunction with an inferior or posterior left ventricular infarction. Caused by occlusion of the right coronary artery or left circumflex artery.
Clinical Manifestations
Chest pain dyspnoea, cool, moist skin, nausea and vomiting, extreme weakness and tiredness, pulse becomes rapid and weak, the BP falls but may be elevated in the 1ยบ few hours, elevation of body temperature, feeling of helplessness, severe anxiety.
Diagnostic evaluation
Patient history.
ECG
Serum enzymes
1. Creatine Kinase and its isoenzymes.
2. Lactic dehydrogenase and its isoenzymes.
3. Aspartate aminotransferase (AST)
Medical Management
Aim-Protection of ischemic and injured heart tissue to preserve muscle function, reduce the infarct size and prevent death.
1. Oxygen therapy improves oxygenation to ischemic heart muscle.
2 Pain control
(a) Opiate analgesic therapy
Morphine relieves pain, (reduces preload and after load) and relieve anxiety.
Meperidine (Demerol) used when patient is allergic to morphine or sensitive to respiratory depression.
(b) Vasodilator therapy
Nitro-glycerine (Sub Dermal, IV, Paste) promotes venous and arterial relaxation as well as relaxation of coronary vessels and prevention of coronary spasm.
(c) Anxiolytic therapy
Benzodiazepines used when anxiety complicates chest pain.
Pharmacologic Therapy
(a) Thrombolytic agents such as tissue plasminogen activator (Activase) streptokinase (Streptase) - dissolves the thrombus IV/intracoronary.
(b) Adjunctive therapy To prevent fibrinogen from adhering to activated platelets epifibatide (Integrilin) or abciximab (Reopro). To prevent platelet activation e.g. aspirin.
(c). Anticoagulation therapy Heparin.
(d). Beta-adrenergic blocking agents improves oxygen supply and demand, promotes blood flow in the small vessels of the heart.
(e) Antidysrhythmic therapy
(f) Calcium channel blockers improve the balance between oxygen supply and demand by decreasing HR, , antiemetics. Rand BP and dilating coronary vessels. E.g. Diltiazem
Nursing Management
1. Provide a semi-fowler's position [rest, adequate, chest excursion, increase available oxygen and decrease cardiac work].
2. Administer oxygen [to increase oxygen supply].
3. Administer NTG, and morphine, based on vital signs and pain relief (alleviates pain).
4. Monitor BP, HR and RR before and 10-15 minutes after administering nitrates.
5. Continuous cardiac monitoring [increase in HR may indicate heart block].
6. Administer and monitor thrombolytic therapy relieves coronary occlusion.
7. Monitor signs of bleeding, avoid unnecessary venous or arterial punctures. [Thrombolytic cause clot lysis, may bleeding].
8. Administer IV fluids as ordered [IV necessary to compensate for decreased venous return caused by nitrates and morphine].
9. Monitor for signs of LVF (LVF may develop as a result of decreased myocardial contractility and/or administration of excess IVF)
10. Monitor urine output hourly (30nil/hour) [decrease in urine output and indicates a decrease in renal blood flow].
11. Monitor mental status (alertness and orientation) [A change in mental status may indicate a decrease in cardiac output.
13. Administer vasopressors, titrate to BP response.
14. Explain equipment, procedures and need for frequent assessment. Provide support and reassurance to patient and family decreases anxiety.
15. Observes for symptoms of anxiety increase HR, BP and RR - anxiety ->> increase sympathetic activity increase cardiac work.
16. Administer diazepam as prescribed aids decrease anxiety.
17. Offer back massage touch and massage promotes relaxation and improves skin integrity.
18. Take body temperature every 4 hours [as patients can develop increase in temperature within 24-48 hours due to tissue necrosis).
19. Monitor skin color and temperature (cool, clammy skin and pallor associated with vasoconstriction).
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