Chapter 28 Management of Patients With Myocardial Infarction Dr. Maysoon S. Abdalrahim

Pathophysiology: Myocardial Infarction Unstable angina rupture of an atherosclerotic plaque  reduced blood flow in a CA (not completely occluded)  preinfarction angina. Myocardial infarction plaque rupture and thrombus formation Myocardial ischemia (complete occlusion of CA)  an area of the myocardium is permanently destroyed  myocardial death

Pathophysiology: Myocardial Infarction Other causes of MI= intense imbalance between myocardial O2 supply and O2 demand Vasospasm of a CA decreased O2 supply (bleeding, anemia, or low BP) Increased O2 demand (tacky cardia, thyrotoxicosis, cocaine)

Pathophysiology: Myocardial Infarction The area of infarction develops over minutes to hours. “time is muscle”: the urgency of appropriate treatment to improve patient outcomes. The ECG identifies the type (STEMI, NSTEMI)and location of the MI(ant- inf- post- lat), and the timing (acute- evolving- old). the goals of therapy are to prevent or minimize myocardial tissue death and prevent complications

Clinical Manifestations: Myocardial Infarction Chest pain sudden and continuous despite rest and medication Patients may have sympathetic NS symptoms shortness of breath indigestion, nausea Anxiety cool, pale, and moist skin Tachycardia-tachypnea

Diagnostic Findings: Myocardial Infarction Patient History The symptom History of previous cardiac and other illnesses Family history of heart disease. The risk factors for heart disease

Diagnostic Findings: Myocardial Infarction Electrocardiogram For diagnosing an acute MI. It should be obtained within 10 minutes from the time a patient reports pain or arrives in the ED. serial ECG changes over time, the location, and resolution of an MI. The classic ECG changes are T-wave inversion ST-segment elevation an abnormal Q wave

Electrocardiogram :indicators First myocardial injury signs in ECG is peaked T wave. Then ST elevation more than 1 mm above isoelectric line in two contiguous leads. Then ST depression or T inversion Q wave develop within 1-3 days(0.04sec- 5mm-25% R wave). Poor R wave progrossion

Diagnostic Findings: Myocardial Infarction patients are diagnosed with one of the forms of ACS: Unstable angina : typical symptoms, but ECG & cardiac markers shows no evidence of acute MI. STEMI: ECG evidence of acute MI(changes in two leads) NSTEMI: elevated cardiac biomarkers but no definite ECG evidence of acute MI. During recovery from an MI, the ST segment is the first ECG indicator to return to normal (1 to 6 weeks). Q-wave changes are permanent. T large for 24 hr then inverts within 1-3 days to 2 weeks

Diagnostic Findings: Myocardial Infarction Echocardiogram to evaluate ventricular function when the ECG is nondiagnostic. Detect hypokinetic and akinetic wall motion Determine EF%

Diagnostic Findings: Myocardial Infarction Laboratory Tests Cardiac enzymes and biomarkers to diagnose an AMI. myoglobin and troponin: analyzed rapidly Creatine Kinase and Its Isoenzymes: CK-MB increase within a few hrs and peaks within 24hrs Myoglobin: a heme protein (transport O2). starts to increase within 1 to 3 hrs and peaks within 12 hrs, not very specific for cardiac. Troponin: a protein regulates the myocardial contraction that have 3 isomers : C, I, and T. (I&T)reliable and critical markers of MI. detected within a few hrs and remains elevated for 3 weeks

Diagnostic Findings: Myocardial Infarction

Diagnostic Findings: Myocardial Infarction Cardiac Catheterization(in less than 60 min)

Medical Management: Myocardial Infarction The goals are to minimize myocardial damage, preserve myocardial function, and prevent complications. These goals are facilitated by the use of guidelines developed by the American College of Cardiology (ACC) and the AHA (Chart 28-7).

Medical Management: Myocardial Infarction Pharmacologic Therapy aspirin, nitroglycerin, morphine, an IV beta-blocker, and other medications Patients should continue the beta-blocker throughout hospitalization LMWH + platelet-inhibiting agents to prevent further clot formation. NSAIDS may be discontinued because of SE on heart. Analgesics: morphine in IV boluses :reduce pain& anxiety, preload & afterload, which decrease load on heart & relax bronchioles(↓BP, ↓RR)

Medical Management: Myocardial Infarction Pharmacologic Therapy Angiotensin-Converting Enzyme Inhibitors (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II BP decreases and diuresis (decrease O2 demand).so check BP-↑K-fluid balance-↓Na-UOP- KFT. Thrombolytics: IV in a specific protocol (Chart 28-8). The purpose is to dissolve the thrombus in a CA must be administered within 3 to 6 hours for patients with ECG evidence of acute MI, and should be initiated within 30 minutes of presentation to the hospital (door-to-needle time).

Chart 28-8

Medical Management: Myocardial Infarction Emergent Percutaneous Coronary Intervention (PCI) used to open the occluded CA increase O2 supply. should be performed within 60 minutes (door-to-balloon time). Coronary Stent is a tiny wire mesh tube used to prop open an artery during angioplasty. The stent stays in the artery permanently. The stent will also improve blood flow to the heart muscle and will relieve chest pain (angina).

Cardiac Rehabilitation: Myocardial Infarction After the patient with an MI is free of symptoms education, individual and group support, and physical activity. The goal: to improve the quality of life. limit the effects and progression of atherosclerosis return to work and pre illness lifestyle enhance psychosocial and vocational status prevent another cardiac event.

Ng diagnoses Ineffective cardiac tissue perfusion RT reduced coronary blood flow Risk for imbalanced fluid volume Risk for ineffective peripheral tissue perfusion RT decreased COP Anxiety RT cardiac event Knowledge deficiency about ACS self-care

Nursing Interventions: Myocardial Infarction Relieving Pain and Symptoms of Ischemia Balancing O2 supply with O2 demand relief of chest pain is the top priority O2 by nasal cannula in a rate of 2 to 4 L/min, saturation levels of 96% to 100% Medication therapy Vital signs

Nursing Interventions: Myocardial Infarction Relieving Pain and Symptoms of Ischemia Physical rest in bed with the back elevated to decrease chest discomfort and dyspnea. Tidal volume improves Drainage of the upper lung lobes improves. venous return to the heart (preload) decreases

Nursing Interventions: Myocardial Infarction Improving Respiratory Function Regular assessment to detect early signs of pulmonary complications. Monitor fluid volume status to prevent overloading Encourage deeply breathing exercises Change position frequently Pulse oximetry

Nursing Interventions: Myocardial Infarction Promoting Adequate Tissue Perfusion Bed or chair rest to reduce O2 oxygen demand and remain until the patient is pain free and stable. check skin temperature and peripheral pulses frequently to monitor tissue perfusion.

Nursing Interventions: Myocardial Infarction Reducing Anxiety To reduce the sympathetic stress  decrease O2 demand and relieve pain Develop a trust and caring relationship Provide information Ensure a quiet environment, promote sleep, using caring touch, relaxation techniques, using humor, and providing spiritual support An atmosphere of acceptance Music therapy and pet therapy

Nursing Interventions: Myocardial Infarction Monitoring and Managing Complications the Plan of Nursing Care in Chart 28-10. monitor the patient closely for changes in cardiac rate and rhythm, heart sounds, BP, chest pain, respiratory status, urinary output, skin color and temperature, sensorium, ECG changes, and laboratory values. Report rapidly any changes in the patient's condition

Nursing Interventions: Myocardial Infarction Teaching patients self-care. provide adequate education about heart-healthy living facilitate the patient’s involvement in a cardiac rehabilitation program