Acute myocardial infarction

14. Aug 2014

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Acute myocardial infarction

  1. Acute Myocardial Infarction Prepared by: BSN, Level IV Sarah Jane A. Cristobal
  2. Definitions • Is the medical term for an event commonly known as a heart attack. An MI occurs when blood stops flowing properly to a part of the heart, and the heart muscle is injured because it is not receiving enough oxygen. Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious.
  3. Definitions • Myocardial infarction occurs when myocardial ischemia, a diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis. Ischemia at this critical threshold level for an extended period results in irreversible myocardial cell damage or death.
  4. Anatomical Structure
  5. Signs & Symptoms • A person having an acute MI usually has sudden chest pain that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck. • Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety.
  6. • Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64%, the person does not have chest pain or other symptoms. These are called "silent" myocardial infarctions. Signs & Symptoms
  7. Risk factors • Important risk factors are previous cardiovascular disease, old age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, and the use of cocaine and amphetamines.
  8. Physical exam The parts of the physical exam that are most helpful in diagnosing heart failure are: • Measuring blood pressure and pulse rate. • Checking the veins in the neck for swelling or evidence of high blood pressure in the veins that return blood to the heart. Swelling or bulging veins may indicate right-sided heart failure or advanced left-sided heart failure.
  9. • Listening to breathing (lung sounds). • Listening to the heart for murmurs or extra heart sounds. • Checking the abdomen for swelling caused by fluid buildup and for enlargement or tenderness over the liver. • Checking the legs and ankles for swelling caused by fluid buildup (edema). • Measuring body weight. Physical exam
  10. Normal • Lung and heart sounds are normal, blood pressure is normal, and you have no sign of fluid buildup or swollen veins in the neck. • You may have further exams or tests to check for other causes of symptoms.
  11. Abnormal findings that suggest heart failure: • High blood pressure (140/90 mm Hg or above) or low blood pressure is present. Low blood pressure could be a sign of late-stage heart failure. • An irregular heart rate (cardiac arrhythmia)
  12. Abnormal findings that suggest heart failure: • A third heart sound (indicating abnormal movement of blood through the heart) is heard. Heart murmurs may or may not be present. • The impulse normally felt from the lower tip of the heart (apex) is not felt in its normal position on the chest wall, suggesting enlargement of the heart.
  13. Abnormal findings that suggest heart failure: • You have a swollen liver or have pain in the right upper abdomen, loss of appetite, or bloating. This suggests that blood may be backing up into the body. • You have swelling in your legs, ankles, or feet or in the lower back when you lie down, and it is clearly not caused by another condition. Fluid buildup first occurs during the day and goes away overnight.
  14. Abnormal findings that suggest heart failure: • Swollen neck veins or abnormal movement of blood in the neck veins suggest that blood may be backing up in the right ventricle. • Noises (pulmonary rales) such as bubbling or crackling are heard, which may point to fluid buildup in the lungs. Your doctor uses a stethoscope to hear these noises while you take deep breaths.
  15. Diagnostic Procedures • The main way to determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the electrical signals in the heart and testing the blood for substances associated with damage to the heart muscle.
  16. Diagnostic Procedures • . Common blood tests are troponin and creatine kinase (CK-MB). ECG testing is used to differentiate between two types of myocardial infarctions based on the shape of the tracing. An ST section of the tracing higher than the baseline is called an ST elevation MI (STEMI) which usually requires more aggressive treatment.
  17. Diagnostic Procedures • A cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI.
  18. Diagnostic Procedures • Clinical history of ischaemic type chest pain lasting for more than 20 minutes • Changes in serial ECG tracings • Rise and fall of serum cardiac biomarkers • At autopsy, a pathologist can diagnose an MI based on anatomopathological findings.
  19. Pathopysiologic Mechanism Acute myocardial infarction (MI) generally refers to segmental (regional) myocardial necrosis, typically endocardium-based, secondary to occlusion of an epicardial artery. In contrast, concentric subendocardial necrosis may result from global ischemia and reperfusion in cases of prolonged cardiac arrest with resuscitation. Areas of myocardial infarction may be subepicardial if there is occlusion of smaller vessels by thromboemboli originating from coronary thrombi. In the majority of patients, there is obstructive coronary disease at angiography.
  20. Pathopysiologic Mechanism The area of infarct occurs in the distribution of the occluded vessel. Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. There is often extension to the anterior portion of the ventricular septum with proximal left coronary occlusions.
  21. Pathopysiologic Mechanism In hearts with a right coronary dominance (with the right artery supplying the posterior descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct. With a left coronary dominance (about 15% of the population), a proximal circumflex occlusion will infarct the posterior wall; in the right dominant pattern, a proximal obtuse marginal thrombus will cause a lateral wall infarct only, and the distal circumflex is a small vessel.
  22. Pathopysiologic Mechanism The anatomic variation due to microscopic collateral circulation, which is not evident at autopsy, plays a large factor in the size of necrosis and distribution. Unusual patterns of supply to the posterior wall, such as wraparound left anterior descending or posterior descending artery supplied by the obtuse marginal artery, may also result in unexpected areas of infarct in relation to the occluded proximal segment.
  23. Pathopysiologic Mechanism A proximal occlusion at the level of an epicardial artery results in a typical distribution that starts at the subendocardium and progresses towards the epicardium (the so- called wavefront phenomenon).[1] Therefore, an area of necrosis or scarring is considered to have an "ischemic pattern" if it is largest at the endocardium, with a wedge-shaped extension up to the epicardial surface.
  24. Pathopysiologic Mechanism Ischemic injury, however, may be located in the mid myocardium or even the subepicardium if the level of the coronary occlusion is distal within the myocardium. Therefore, in cases of thromboemboli from epicardial thrombi (especially plaque erosions), there may be patchy infarction, often associated with visible thrombi within the myocardial vessels, not centered in the endocardium but occurring anywhere in the myocardium, including midepicardial and subepicardial locations
  25. Complications of AMI Reperfusion injury Acute heart failur Aneurysm of heart Cardiac muscle cells rupture BBB or RBBB Ventricular arrhytmias: Fibrilation Bradhyarrhytmia Cardiogenic shock Hypovolemia
  26. Pharmacologic treatment • An MI requires immediate medical attention. Treatment attempts to save as much viable heart muscle as possible and to prevent further complications, hence the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI.
  27. Pharmacologic treatment • Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit. An MI requires immediate medical attention. Treatment attempts to save as much viable heart muscle as possible and to prevent further complications, hence the phrase "time is muscle".
  28. Pharmacologic treatment • Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit.
  29. Other Lifestyle Changes and Other Therapies •Smoking should always be discouraged. •Pneumococcal and influenza immunization may reduce the incidence of respiratory infections that may worsen HF.
  30. Other Lifestyle Changes and Other Therapies •Continuous positive airway pressure (CPAP) to improve daily functional capacity and quality of life may be used in patients with HF and obstructive sleep apnea. •Non-pharmacologic techniques for stress reduction may be considered as a useful adjunct for reducing anxiety in patients with HF.
  31. Nursing Diagnosis 1. Decreased Cardiac Output related to: changes in the frequency of heart rhythm. 2. Impaired Tissue Perfusion related to: decrease in cardiac output. 3. Ineffective Airway Clearance related to: accumulation of secretions.
  32. Nursing Diagnosis 4. Ineffective Breathing Pattern related to: lung development is not optimal. 5. Impaired Gas Exchange related to: pulmonary edema. 6. Acute Pain relate to: increase in lactic acid. 7. Fluid Volume Excess related to: retention of sodium and water.
  33. Nursing Diagnosis 8. Imbalanced Nutrition, Less Than Body Requirements related to: Inadequate intake. 9. Activity Intolerance relate to: imbalance between myocardial oxygen supply and needs. 10. Self-Care Deficit related to: physical weakness.
  34. Nursing Intervention • Administer analgesics as ordered. • Organize patient care and activities to allow periods of uninterrupted rest. • Provide a clear liquid diet until nausea subsides. • Provide stool softener to prevent straining during defecation.
  35. Nursing Intervention • Assist with range of motion exercises. • Provide emotional support, and help reduce stress and anxiety. • Assess and record the patient’s severity, location, type, and duration of pain. • Check his blood pressure after giving nitroglycerin, especially during first dose.
  36. Nursing Intervention • Thoroughly explain the medication and treatment regimen. • Review dietary restriction with the patient. • Advise the patient about appropriate responses to new or recurrent symptoms. • Stress the need to stop smoking.
  37. Nursing Intervention Psychological and social support • Patients should be offered basic stress management advice and may not need more complex treatment such as cognitive behavioural therapy.
  38. Nursing Intervention • Psychological and social support However, one study found that six components of psychological intervention - usual care, educational, behavioural, cognitive, relaxation and support - offered positive benefits in terms of clinical outcomes
  39. Nursing Intervention Psychological and social support • Partners and carers should be involved if this is in accordance with the patient's wishes. • Patients with anxiety or depression should be managed according to the appropriate NICE guidance.
  40. Discharge planning Medicines management plan • Consider starting guideline-recommended medicines in hospital before discharge. • Provide all patients with a written medicines management plan which includes: – a list of all medicines – the dose and plan for any required dose titration – intended duration of therapy – the purpose and potential benefits of therapy – potential adverse effects of each medicines – schedule for follow-up and monitoring – access to consumer medicine information.
  41. Discharge planning • provide smoking-cessation advice and support to all patients who smoke • Smoking is one of the most significant risk factors • for cardiovascular disease, including myocardial infarction (MI). • Stopping smoking is associated with a substantial reduction in risk of all-cause mortality among patients with coronary heart disease.