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Disruption(s) - Myocardial Infarction (MI)

Bullet Points: Pathophysiology/Etiology Acute Coronary Syndrome includes Ustable Angina, NSTEMI AND STEMI Result of sustained ischemia Causes irreversible myocardial cell death Necrosis of the entire thickness of myocardium takes 4 to 6 hours The degree of altered function depends on the area of the heart involved and the size of the infarct Contractile function of the heart is disrupted in areas of myocardial necrosis Most MIs involves the left ventricle (LV) 55-70 Contractile ejection fraction How effectively the heart can pump blood with each beat. Less than 40 indicated heart failure and needs to be on long term ACE inhibitors Less than 35% IS LIFE THREATENING Risk Factors Diabetes Arthrosclerosis More men than women Highest among white middle aged men Occlusion of the coronary arteries Pain Total occlusion anaerobic metabolism and lactic acid accumulation Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration EMERGENCY Commonly occurs in the early morning hours Pain lasting more than 20 minutes Not feeling right Low energy GI disruptions Nausea and vomiting can result from reflex stimulation of the vomiting center by severe pain Fever systemic manifestation of the inflammation process. May increase in the first 24hours. May last as long as one week. SOB Weakness easy fatigue Color may change to ashen because of the release of catecholamines into the blood stream because of ischemic cells Ashen, clammy, cool to the touch and diaphoretic Initially increase HR and BP and the decrease of BP secondary to decrease in cardiac output Crackles and Jugular Vein Distention Abnormal heart sounds S3 or S4 sounds New murmur Something different and change in heart sounds Healing begins within 24 hours and leukocytes infiltrate the area of cell death Development of collateral circulation Necrotic zone identifiable by ECG changes and nuclear scanning 10-14 days after MI, scar tissue is still weak and vulnerable to any kind of stress By 6 weeks after MI, scar tissue has replaced necrotic tissue

Clinical Manifestations (Subjective and Objective)

Treatment(s) and Treatment Goals

Complications:

Ventricular Remodeling Process of the normal myocardium becoming hypertrophied and dilated in an attempt to compensate for the infarcted muscle. Continuous ongoing monitoring Treatment of choice for confirmed MI Balloon angioplasty and tents Fibrinolytic therapy Indications and contraindications (surgery, liver disease, ulcerative colitis: Anything where bleeding is involved); best marker of reperfusion: Return of ST segment to baseline, Rescue PCI if thrombolysis fails, major complication: Bleeding. Must be used within 6 hours of the verified acute MI Coronary surgical revascularization Sometimes fails, presence of left main coronary artery or three-vessel disease (patient will have a CABG), failed PCI with ongoing chest pain, history of diabetes mellitus CABG uses arteries and veins for grafts usually uses the mammary artery. Need to get past the blockage so patient can have adequate perfusion. Increased afterload and better cardiac output. Continuous ECG monitoring, endotracheal tube, mechanical ventilation (extubation within 12 hours), Pacing wires for emergency pacing of the heart, NOP, NG tube for gastric decompression, Urinary catheter MIDCAB alternative to traditional CABG Dont need to be on heart lung bypass Coronary surgical revascularization Off-pump

Dysrhythmias Most common complication, present in 80% of MI patients Most common cause of death in the pre-hospital period. Occur most often with anterior wal infarction, HF, or shock Life-threatening anterior MI, heart failure or shock Heart Failure Occurs when the pumping power of the heart has diminished. Signs include mild dyspnea, restlessness, slight tachycardia, agitation, pulmonary congestion on chest x-ray, S3 or S4 heart sounds, cracks, and jugular vein distension. Cardiogenic shock not adequate O2 being supplied to the tissue. Because of severe LV failure. Requires aggressive management arrhythmias supraventricular tachycardia/bradycardia Chest pain, diaphoretic, restlessness and confusion, SOB. Low BP and necrotic tissue Goal of therapy is to maximize O2 delivery, reduce O2 demand, and prevent complications such as acute renal failure Papillary Muscle Dysfunction May occur if the infarcted area includes or is adjacent to the papillary muscle that attaches to the mitral valve. It causes mitral valve regurgitation, which increases the volume of blood in the left atrium. Reduces CO. Suspect this if you auscultate a new systolic murmur at the cardiac apex. Echocardiogram confirms the diagnosis. Immediate Mitral valve replacement is needed Ventricular aneurysm Results when the infarcted myocardial wall is thin and bulges out during contraction. May experience HF, dysrhythmias, and angina. May lead to ventricular rupture and may harbor thrombi that can lead to an embolic stroke Acute pericarditis An inflammation of visceral and/or parietal pericardium. Hear a pericardial friction rub which may be auscultated at the mid to lower sternal border. May result in cardiac compression, decreased ventricular filling and emptying, and HF. Occurs 2 to 3 days after an acute MI as a common complication. Chest pain that is aggravated my inspiration, coughing and movement of the upper body characterizes pericarditis. Sitting in a forward position often relieves the pain. Diagnosis is made with a 12-lead ECG. Pain relief with aspirin or corticosteroids Dressler syndrome Pericarditis with effusion and fever that develops 4 to 6 weeks AFTER MI chest pain, pericardial friction rub may be heard on auscultation, pericardial effusion and arthralgia May also occur after cardiac surgery. Lab findings show an elevated WBC count and sedimentation rate. Short term corticosteroids are used to treat.

Diagnostic Studies Describe how the test/study Prep required before study: Post-study patient care: Name of Test is performed: 1.Detailed health history and physical 2. 12 lead ECG: Changes Changes in the QRS complex, No prep If initial reading is non in QRS complex, ST St segment, and T wave caused diagnostic, serial 12-lead ECgs segment, and T wave can by ischemia and infarction. are done every 2 to 4 hours. rule out or confirm UA or MI UA or NSTEMI usually have transient thrombosis or incomplete coronary occlusion and usually dont develop pathologic Q waves STEMI patients tend to have a more extensive MI that is associated with prolonged and complete coronary occlusion and the development of a pathologic Q wave on the ECG 3. Serum cardiac markers Released into the blood from cardiac enzymes and necrotic heart muscle after an troponin MI. Indicates cardiac damage. 4. Coronary angiography Evaluates the extent of the disease and to determine the most appropriate therapeutic modality (this is the only way to confirm diagnosis of Prinzmetals angina)

5. Stress testing, 6. Echocardiogram 7. C reactive protein test 8. Troponin level test Peaks within hours and can be detected for up to 2 weeks 9. CK-MB test it rises within 6 hours after necrotic tissue 10. Additional Considerations: Medications: Steroids Morphine Pain and afterload reduction IV nitroglycerin afterload reduction and managing Patient Teaching Nutritional therapy mono saturated oils Include sexual counseling,

pain Statin Beta Blockers Ace Inhibitors Ant dysrhythmia drugs Stool softeners Cholesterol lowering drugs Tissue plasminogen activator (t-PA) Oxygen at 4L

Physical activity May use the Metabolic equivalent (MET) to identify levels of physical activity. 1 MET is the amount of O2 needed by the body at rest 3.5 mL of O2 per kilogram per minute or 1.4 cal/kg of body weight per minute. The MET determines the energy costs of various exercises. S/S of angina and MI and what to do should they occur When and how to seek help Anatomy and physiology of the heart and coronary arteries Cause and effect of CAD Definition of terms Identification of and plan to decrease risk factors Rational for tests and treatments, activity limitations/rest, diet, and medications Appropriate expectations about recovery and rehab Measures to take to promote recovery and health Importance of the gradual, progressive resumption of activity. -------------------------------------------------------------------------Nursing Management Establish an IV route to provide access for emergency drug therapy Initiate O2 by nasal cannula at a rate of 2-4L/min and ECG monitoring, Sublingual NTG and aspirin (chewable) Morphine sulfate is given IV for pain Monitor vital sighns, including pulse Ox frequently during the first few hours after admission and closely thereafter. Maintain bed rest and for a few weeks.