Sunday, September 03, 2006

Myocardial Infacrtion

Myocardial infarction reffers to the process by which myocardial tissue is destroyed in regions of the heart that are deprived of their blood supply after closure of the coronary artery or one of its branches, either by a trhombus or through obtruction of the vessel lumen by atherosclerosis. Arterial hypertention and diabetes are also underlying causes.
Preventive Measures
Epidemiological studies and observations by cardiologists reveal that there are coronary risk factors that tend to make an individual more prone to develope coronary heart disease. This information is important in the prevention of premature coronary heart disease as well as forestalling recurring episodes in patients with known atherosclerotic disease.
These factors include as a following:
  • Hypercholesterolemia, elevated blood lipid
  • Hypertension
  • Elevated Blood Glucose (Diabetes Mellitus)
  • Obwsity
  • Habitual dietary intake of excessive calories, total fats, cholesterol, carbohydrates and salt.
  • Physical inactivity
  • CAD
  • Thrombus formation
  • Cigarette smoking
  • Positive family history
  • Symptom and Sign

    The patient with myocardial infarction is usually male, is over 40 and has arterosclerosis of coronary vessel and often arterial hypertention. However, the patient my be in his early 30's or even 20's. In typical patient, the pain start suddenly, usually over the lower sternal region and upper abdomen, and is continous more than 30 minutes with the pain character such as crushing, vise-like, griping, but it may increase steadily in severity until it become almost unbeareable.
    It is heavy vise-like pain, which may radiate to the shoulders and down the arms, usually in the left arm. Unlike the pain of true angina, it become spontaneously (not following effort, emotional upset, etc), persist for hour of days, and is releived neither by rest nor by nitrites. The palse may become very rapid, irregular, and feeble, even imperceptible , and the heart may dilate. Gallp rhythm (accentualed third heart sound making the three heart sound similar to those of galloping horse) often developes.
    The person with a severe occlusion may be in shock , his color is ashen, he break out in clammy sweat, vomiting is commond. In a few hours his temperature rises, blood presure falls to an unusually low point, the leucocyte count rises to 15,000 or 20,000 enzymes are elevated and can be correlated with the patien's clinical corse. The creatinine phosphokinase (CPK) may rise 5 to 10 times or more and is especialy diagnostic for heart muscle damage. Changes may be seen in the electrocardiogram within 2 to 12 hours (but may take as long as 72 to 96 hours). When ECG change as eleveted S-T segment and inverted T waves confim that an acute myocardial infarction. Even the ECG is normal, elevation of serum enzymes reveal that caution is indicated in the handling of the patient.
    Medical and Nursing management
    The most critical period of the patient with myocardial infarction is durinh the first 48 hours following the attack. Cardiogenic shock, ventricular fibrillatio, and cardiac arrest are common cause of sudden deaths during this time period , therefore nurse care must be do as a following actions:

    1. Acute condition, place patient in Ssemi Fowler Position, bed rest
    2. Nasal O2 to reverse as much ischemia as possible
    3. Establish a patient IV line
    4. Provide pain relief, morphine sulfate IV(given IV because after in infarction there is poor peripheral perfusion and because serum enzymes would be affected by IM injection) as doctor orderMonitor ECG and haemodinamic procedures.
    5. Administer antiarrhythmias as order.
    6. Perform complete lung/cardiovasculer assesment
    7. Monitor urine output and report output of less than 30 ml/hour; indicates decrease cardiac output.
    8. Maintain full liquid diet with gradual increase to soft; low sodium.
    9. Maintain quiet environment.
    10. Administer stool softeners as ordered to fasilitate bowel evacuation and prevent straining.
    11. Relieve associate with coronary care unit (CCU) environnment.
    12. Administer anticoagulants as order>
    13. Administer thrombolyitics (tissue -type plasminogen activator or t-pa and streptokinase) and monitor for side effects; bleeding.

    If the doctor incharge permitted to the patient for discharge, the nurse must be take responsible as a below:

    1. Teach about effects of MI, healing proces, and treatment regimen
    2. Medication regimen including name, purpose, schedule, dosage, side effects.
    3. Risk factors, with necessary lifestyle modification
    4. Dietary restrictions; low sodium; cholesterol; avoidance of caffeine
    5. Importance of participation in a progressive activity program
    6. Resumption of sexsual activity according to physician's orders(usually 4-6 weeks)
    7. Need to report the following symptom: increased persistent chest pain, dypsnea, weakness, fatigue, persisten palpitations, light-headedness
    8. Enrollment of client in cardiac rehabilitation program


    Anonymous said...

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    Anonymous said...

    I hope you add this info mr. maruf:
    Every year in the United States more than 700,000 patients arrive at the emergency room with ST-segment elevation acute myocardial infarction (STEMI). Their in-hospital, 1-month, and 1-year mortality is high. For a internist-cardiologist standing at the bedside of a critical patient with STEMI, the ultimate goal is to open, as quickly as possible, the acute infarct-related artery (IRA) and to turn the clinically volatile situation into controlled recovery without ventricular remodeling. With the advent of thrombolytic therapy (TT) and primary coronary interventions (PCIs), there came a great opportunity to open acutely occluded IRA and restore antegrade flow to the ischemic myocardium. The strategies which guide the cardiologist from the first encounter with the patient in the emergency room through the discharge day and the office follow-up ten years later
    From the angiographic point of view, successful reperfusion is defined as early and complete restoration of coronary blood flow to a thrombolysis in acute myocardial infarction (TIMI) 3 flow [1]. This brisk flow allows sufficient microvascular perfusion to result in significant reduction in mortality.

    Evidence-based Medicine: DES for STEMI – The TYPHOON trial
    712 patients with STEMI randomized between Cypher stents, and balloon angioplasty and bare metal stent (BMS). The results showed that at 1 year, the rate of mortality was 2.2% for both groups. The overall rate of targetvessel failure was 7.3% for the Cypher stent and 14.3% among those treated with balloon angioplasty and a BMS (a 49% relative reduction). In a sub-study with 210 patients, there was 83% reduction in the rate of re-stenosis and an 83% reduction in tissue proliferation. The stent thrombosis rate was 3.4% for DES and 3.6% for POBA or BMS. These results met the expectations of low mortality and excellent long term major adverse cardio-vascular events (MACE)

    pammi said...

    Stent has proved to be a life saving tube for cardiac patient which is used in angioplasty surgery. The tube is a tiny, expandable, mesh-like tube made of a metal such as stainless steel or cobalt alloy. A cardiac stent is a small tube that is used to widen arteries supplying the heart that have narrowed. Stent for heart is sold by different companies in the world.Stent for heart