CARE OF PATIENTS WITH MYOCARDIAL INFARCTION

CARE OF PATIENTS WITH MYOCARDIAL INFARCTIONPrepared by: Moonyeen Natanawan

OPENING PRAYER

Review of Anatomy and PhysiologyVIDEO PRESENTATION

Definition of disease conditionAcute Myocardial infarctionOccurs as a result of sustained ischemia, causing irreversible myocardial cell death (necrosis). When a thrombus develops, perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis. Contractile function of the heart stops in the necrotic areas. The degree of altered function depends on the area of the heart involved and the size of the infarction. Most MIs involve some portion of the left ventricle. Definition of termsAtherosclerosis- an abnormal accumulation of lipid, or fatty substances, and fibrous tissue lining of the arterial blood vessels walls.Ischemia- insufficient tissue oxygenation Infarction- an area of necrosis in a tissue or organ resulting from obstruction of the local circulation by a thrombus or embolus Angina pectoris- chest pain brought by myocardial ischemia. High-density lipoprotein (HDL)- a protein-bound lipid that transports cholesterol to the liver for excretion in the bile; composed of a higher proportion of protein to lipid than low-density lipoprotein; exerts a beneficial effect on the arterial wall. Low-density lipoprotein (LDL)- a protein bound lipid that transports cholesterol to tissues in the body; composed of a lower proportion of protein to lipid than high-density lipoprotein; exerts a harmful effect on the arterial wall.

Classification of InfarctionTransmuralWith necrosis through the wall of the myocardium. They occur with almost a 40% frequency and are usually associated with occlusion of an epicardial artery. NontransmuralIt occurs in the inner half of the endocardial myocardium; they occur with 60% frequency.

Site of infarctionAnteriorIt usually involves occlusion of the left anterior descending (LAD) artery. Minimal involvement includes the apical half of the left ventricle.Inferior-posteriorInferior and posterior MIs result from occlusion of the RCA in 80% to 90% of the patients, and occlusion of the LCA in 10% to 20% of the patients

LateralMI confined to the lateral wall of the left ventricle is the least common and is usually due to occlusion of the LCA.Right ventricularIsolated right ventricular MIs compose from 3% to 8% of MIs, whereas in patient with inferoposterior MIs up to one-third may have concomitant RV infarction. None-Q waveOccurs in 25% to 35% of all MIs and more frequently occurs in women and the elderly. In non-q wave infarction, as in Q wave infarction, the morphologic lesion usually involves disruption of the atherosclerotic plaques, resulting in thrombus formation. Concept MapRisk FactorsClinical manifestationsDiagnostic examsMedical managementSurgical managementNursing managementRehabilitation Complications

Risk factorsPredisposing FactorsFamily historyA history of MI in one first-degree relative doubles, and in two or more first-degree relatives triple MI risk. MI risk is strongest when MI in relatives occurs before age 55 but is still present when MI occurs after age 55. Increasing ageOlder persons are at risk for hypertension than younger persons. The aging processes that increase BP include stiffening of the arteries, decreased baroreceptor sensitivity, increased peripheral resistance and decreased renal blood flow.African American

Precipitating factorsCigarette smoking Cigarette smoking causes more deaths from CHD (MI and sudden cardiac attack) than from either lung cancer or COPD. Hypertension(systolic blood pressure of at least 140 mmhg or diastolic blood pressure of at least 90 mmhg) carries particular importance as a cardiovascular outcomes, and control of high blood pressure is known to decrease its risk

Serum lipids and lipoproteinsElevated serum total cholesterol and low-density lipoproteins cholesterol (LDL) are associated with an increase risk of CHD in men and women across the age span.

Diabetes mellitusDoubles the rate of MI in men, and increases the rate of MI in women four to six fold. Ischemic heart disease mortality is double in men with diabetes and tripled in women with diabetes.

Obesity and weight changeIn the Framingham study, men under the age of 50 who were greater than 30% above ideal weight (determined by metropolitan life insurance tables) had double the incidence of CHD and acute MI compared with those less than 10% above the ideal weight.Oral contraceptivesIn the early studies, OC use was associated with an increased risk of nonfatal and fatal MI in young women.

Clinical manifestationAngina pectorisIs a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest.

Typical chest pain in acute myocardial infarction has the following characteristics:

Intense and unremitting for 30-60 minutes

Retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left arm

Usually described as a substernal pressure sensation that also may be characterized as squeezing, aching, burning, or even sharp

In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gasArrhythmiaIncrease response of catecholaminesWeakness/Fatigue

HypertensionIn response to the release of catecholamines, the BP and HR may be elevated.

Nausea and VomitingCan result from reflex stimulation of the vomiting center by the severe pain. FeverThis increase of temperature is a systemic manifestation of the inflammatory process caused by myocardial cell death.

Diagnostic examsElectrocardiogram (ECG)The 12- lead ECG provides information that assist in ruling out or diagnosing an acute MI. It should be obtained in 10 minutes from the time a patient reports pain or arrives in an emergency department.

There are typical changes to the normal pattern of the heart tracing in MI. Patterns that occur include things called pathological Q waves and ST elevation. However, it is possible to have a normal ECG even if you have had an MI

Echocardiogram uses sound waves to produce images of your heart. During an echocardiogram, your doctor can determine whether all parts of the heart wall are contributing normally to your heart pumping activity.

Blood tests.

A blood test that measures a chemical called troponin is the usual test that confirms MI. This chemical is present in heart muscle cells. Damage to heart muscle cells releases troponin into the bloodstream. In MI the blood level of troponin increases within 3-12 hours from the onset of chest pain, peaks at 24-48 hours, and returns to a normal level over 5-14 days.

Laboratory tests used in the diagnosis of myocardial infarction include the following:

Cardiac biomarkers/enzymes: The American College of Cardiology/American Heart Association (ACC/AHA) guidelines on unstable angina/NSTEMI (nonST-segment elevation myocardial infarction) recommend that in patients with suspected myocardial infarction, cardiac biomarkers should be measured at presentationTroponin levels: Troponin is a contractile protein that normally is not found in serum; it is released only when myocardial necrosis occursCreatine kinase (CK) levels: CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hoursMyoglobin levels: Myoglobin is released more rapidly from infarcted myocardium than is troponin; urine myoglobin levels rise within 1-4 hours from the onset of chest pain

Complete blood countChemistry profileLipid profileC-reactive protein and other inflammation markers

Stress testIf your sign and symptoms occur more often during exercise, your doctor may ask you to walk on a treadmill or ride a stationary bike during an ECG. This is known as an exercise stress test. Angiogram or Cardiac catheterizationTo view blood flow through your heart, your doctor may inject a special dye into your arteries (intravenously). CT scancan help doctor visualize your arteries. An ultrafast CT scan, can detect calcium within fatty deposits that narrow coronary arteries

Medical managementNitroglycerin- widens arteries Aspirin- can prevent blood clot Beta blockers-improve blood flow Ace inhibitors- improve survival after heart attack Lipid management- helps control cholesterol t Surgical managementPercutaneous Transluminal Coronary Angioplasty A balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemiaCoronary Artery stent A stent is a metal mesh that provides structural support to a vessel at risk of acute closure. The stent is positioned over the angioplasty balloon

Atherectomy Is an invasive interventional procedure that involves the removal of the atheroma, or plaque, from a coronary artery by cutting, shaving, or grinding. It may be used as a conjunction with PTCA.BrachytherapyReduces the recurrence of obstruction, preventing vessel restenosis by inhibiting smooth muscle cell proliferation. Traditional coronary artery bypass graft

ATHERECTOMYNursing management/Rehabilitation

Complications Dysrhythmias Most common complication after an MI is dysrhythmias, which are presenting 80% of MI patients. Its caused by any condition that affects the the myocardial cells sensitivity to nerve impulses, such as ischemia, electrolyte imbalances, and sympathetic nervous system stimulationHeart Failure It occurs when the pumping power of the heart has diminished. Cardiogenic shock Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe left ventricular failure. Papillary muscle dysfunction Occurs when inadequate oxygen and nutrients are supplied to the Papillary muscle dysfunction May occur if the infracted area includes or is adjacent to the papillary musclet hat attaches to the mitral valve. Papillary muscle dysfunction causes mitral valve regurgitation, which increases the volume of blood in the left atrium.

Ventricular Aneurysm Results when the infracted myocardial wall becomes thinned and bulges out during contractionPericarditis Is an inflammation of the visceral and/or parietal Pericardium, may result in cardiac compression, Decreased ventricular filling and emptying, and HF out during contraction.Dressler syndrome Is characterized by pericarditis with effusion and fever that develops 4 to 6 weeks after MI. ResourcesBrunner and Suddarths Textbook of Medical-Surgical Nursing. 11th ed. Lipincott, Williams & Wilkins.Susan Woods and Ericka Froelicher Teekbook of Cardiac Nursing. 3rd edition. J.B. Lippincott companyhttp://www.blackwellpublishing.com/content/bpl_images/content_store/sample_chapter/1405113278/sample%20of%20aaronson.pdfSmeltzer, S. C. & Bare, B. G. (2008). Brunner & Suddarths Textbook of Medical-Surgical Nursing. (11th ed.). Philadelphia: Lippincott Williams & Wilkins.Brunicardi, F.C., et. al. . (2005). Schwartzs Principles of Surgery. (8thed.). United States: McGraw-Hill.Doenges, M.E. (2009). Nurses Pocket Guide. (9th ed.). Philadephia: F.A. Davis CompanyBlack, J.M., & Hawks, J.H. (2009). Medical-Surgical Nursing: Clinical Management for Positive Outcomes. (8thed.). United States: SaundersElsevier.Marieb, E.N. and Hoehn, K. (2007). Human Anatomy & Physiology. (7th ed.). Pearson EducationCuevas Public Health Nursing in the Philippines. 10th edition. 2007Daviss Drug guide for nurses. 11 edition. F.A Daviss company