Google

MYOCARDIAL INFARCTION

The formation of localized necrotic areas within the myocardium. MI usually follows sudden coronary occlusion and the abrupt cessation of blood and oxygen flow to the heart muscle.

Prolonged Ischemia lasting more than 35 to 45 minutes produces irreversible cellular damage and necrosis of the myocardium.

Pathophysiology:

1. Ischemic injury evolves over several hours toward complete necrosis and infarction.
2. Ischemia almost immediately alters the integrity and permeability of the cell membrane to vital electrolytes, thereby decreased myocardial contractility.
3. The autonomic nervous system attempts to compensate for the depressed cardiac performance. This results to further imbalance between myocardial Oxygen supply and demand.
4. MI almost always occurs in the left ventricle and often significantly depresses left ventricular function. This is due to occlusion of the LADA (left anterior descending artery). This is referred to as anterior wall infarction.
5. Alterations in function depend on the size and location of an infarct.
6. Contractile function in the necrotic area ceases permanently.
7. The three areas, which develop in MI, are as follows:
  • Zone of infarction which records pathologic Q wave in the ECG.
  • Zone of injury which gives rise to elevated ST segment
  • Zone of ischemia which produces inversion OCT wave.
8. MI may be classified as follows'
  • Transmural infarct, which extends from endocardium to epicardium.
  • Subendocardial infarct, which affects the endocardial muscles; and
  • Intramural infarction, which is seen in patchy areas of the myocardium and is usually associated with longstanding angina pectoris.
9. Healing requires formation of scar tissues that replace the necrotic myocardial muscle; scar tissue inhibits contractility.

CLINICAL MANIFESTATIONS OF MYOCARDIAL INFARCTION
1. Pain
  • Crushing, severe, prolonged, unrelieved by rest or nitroglycerine; often radiating to one or both arms, the neck and the back.
  • Characterized by “Levine’s sign”
  • Pathophvsiologic Basis: Cessation of blood supply to myocardium caused by thrombotic occlusion causes accumulation of metabolites within ischemic part of myocardium, this affects nerve endings.
2. Anxiety and Apprehension
  • Feeling of "doom," restlessness
  • Pathophysiologic Basis: Severe pain of a heart attack as terrifying; most clients are aware of the significance of a heart attack, restlessness results from shock and pain.
3. Shock
  • Systolic pressure below 8OmmHg, gray, facial color, lethargy, cold
  • diaphoresis, peripheral cyanosis, tachycardia/bradycardia, weak pulse.
  • Patbophysiologic Basis: This may be due to severe; pain, severe reduction in cardiac output and inadequate tissue perfusion, thereby tissue hypoxia.
4. Oliguria
  • Urine flow of less than 30 mI/hr.
  • Pathophysiologic Basis: This indicates renal hypoxia due to inadequate renal tissue perfusion
5. Fever
  • Slight elevation of temperature occurs within 24 hi-s and extends 3 to 7 days accompanied by leukocytosis and elevated ESR.
  • Pathophysiologic Basis: Fever and leukocytosis result from destruction of rnyocardial tissue and ensuing inflammatory process.
6. Indigestion
  • “Gas pains around the heart” nausea and vomiting
  • Pathophysiologic Basis: Client may prefer to believe that pain is caused by "gas" or 'indigestion" rather than by heart disease, nausea and vomiting may result from severe pain or from vasovagal reflexes conducted from an area of damaged myocardium to gastrointestinal tract.
7. Acute Pulmonary Edema
  • Sense of suffocation, dyspnea, orthopnea, gurgling/bubbling respiration
  • Pathophysiologic Basis: Left ventricle becomes severely weakened in pumping action owing to infarction; severe pulmonary congestion results.
8. ECG Changes
  • MI causes elevation of ST segment, inversion of I wave and enlargement of Q wave
  • Pathophysiologic Basis: Pathologic Q wave develops from the area of infarction; elevated ST segment results from the area of injury; and inverted T wave originates from the zone of Ischemia. Elevation of ST segment heralds a pattern of injury and usually occurs as an initial" change in acute MI.
9. Elevated Ck-MB, elevated LDH, elevated AST
  • Pathophysiologic Basis: These cardiac enzymes are produced abnormally large amounts because of cellular damage and death. Elevation of Ck - MB is the most definitive finding in MI, especially in the presence of increased levels of LDH.

COLLABORATIVE MANAGEMENT OF MYOCARDIAL INFARCTION
Medications:
1. Analgesic
2. Thrombolytic therapy
  • To disintegrate blood clot by activating the fibrinolytic processes
  • Streptokinase, urokinase and tissue pIasminogen activator (TPA) are currently used
  • Administration is most crucial between 3 10 6 hrs. after the initial infarction has occurred.
  • Detect for occult bleeding during and after Thrombolytic therapy
  • Assess neurologic status changes, which may indicate GI bleeding or cardiac tamponade.
3. Anticoagulant and anti platelet medications are administered after Thrombolytic therapy to maintain arterial patency.
4. Other medications: Beta - adrenergic blocking agents: diazepam (Valium).

TREATMENT
Goals:
  • Prevention of further tissue injury and limitation of infarct size
  • Maximize myocardial tissue perfusion rind reduce. myocardial tissue demands.
  1. Supplemental oxygen by nasal cannula. This increases myocardial oxygen supply; and relieves pain.
  2. Cardiac monitoring to detect occurrence of dysrythmias.
  3. Percutaneous transluminal Coronary Angioplasty may be done to reopen an occluded artery.
  4. Diet: low cholesterol, tow salt diet is prescribed
  5. Activity: Bed rest is usually prescribed for 24 to 48 hours to decrease oxygen demand. Progressive ambulation is implemented as soon as possible, unless complications occurred.

NURSING MANAGEMENT
  1. Promoting Oxygenation and Tissue Perfusion
  2. Promoting Adequate Cardiac Output
  3. Promote comfort
  4. Providing rest
  5. Promoting Activity
  6. Promoting Nutrition and Elimination
  7. Promoting Relief of Anxiety and Feeling of Well Being
  8. Facilitating Learning
COMPLICATIONS OF MI
  1. Dysrythmias
  2. Cardiogenic shock
  3. Thromboembolism
  4. Pericarditis
  5. Rupture of the Myocardium
  6. Ventricular aneurysm'
  7. Congestive Heart Failures