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![• Severe uncontrolled hypertension on presentation (blood
pressure >180/110 mm Hg)
• History of prior ischemic stroke greater than 3 months
• Known intracranial pathology not covered in contraindications
• Current use of anticoagulants in therapeutic doses
(international normalized ratio [INR] ≥2:3); known
bleeding diathesis
• Recent (within 2–4 weeks) internal bleeding
• Head trauma or traumatic or prolonged (>10 minutes)
• (CPR) or major surgery (<3 weeks)
• Pregnancy/ Dementia/ Active peptic ulcer
Relative Contraindications to Fibrinolytic
Therapy](https://image.slidesharecdn.com/14-acutemyocardialinfarction-230308183912-430f748b/85/14-Acute-Myocardial-Infarction-pdf-49-320.jpg)
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14- Acute Myocardial Infarction.pdf
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- 2. Coronary Arteries • Bloodsupply to the myocardium is by Rt & Lt main coronary arteries. • The left coronary artery branches into; left anterior descending (LAD) & the left circumflex artery (LCA) • The LAD perfuse the anterior two thirds of the ventricular septum, anterior left ventricle & most of bundle branches. • Left circumflex perfuse left lateral & left posterior walls. • The right coronary artery (RCA) perfuse the right ventricle, & the inferior wall of the left ventricle.
- 3. Coronary Atherosclerosis • Atherosclerosisis the abnormal accumulation of lipid deposits & fibrous tissue within Arterial walls & lumen. • In coronary atherosclerosis, blockages & narrowing of the coronary vessels reduce blood flow & decreasing oxygen supply to the myocardium. • The inflammatory response involved with the development of atherosclerosis begins with injury to the vascular endothelium & progress over many years. • Endothelium stop producing the normal Antithrombotic & vasodilating agents. • Symptoms occur with 75% or more occlusion (thanks to the collateral circulation).
- 4. Atherosclerosis—Pathophysiology • Triglycerides, hypertension,& cigarette smoking cause damage to the endothelium. • Fatty substances, cholesterol, cellular waste products, calcium, & fibrin pass are deposited forming lipid plaque (atheroma). • WBC, smooth muscle cells, & platelets to aggregate at the site, forming a fibrous plaque. • The plaque may rupture & a thrombus might form, obstructing blood flow leading to ACS which may result in an AMI.
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- 6. Acute Coronary Syndrome •Unstable angina – Unexpected chest pain/discomfort occurring at rest • MI – ST-segment elevation MI (STEMI) – Non–ST-segment elevation MI (NSTEMI)
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- 8. Copyright © 2018Wolters Kluwer • All Rights Reserved
- 9. Myocardial Infarction (MI) ▪MI is precipitated by an imbalance between oxygen supply & oxygen demand, most commonly R/t a coronary artery thrombosis • Other causes include embolism, anemia, coronary artery spasm, arrhythmias • Thrombus formation occurs most often at the site of an atherosclerotic plaque. • Dysfunctioning endothelium—activation of the inflammatory response---- formation of atherosclerotic plaque --- rupture of plaque --- thrombus formation -- occlusion of the coronary artery --- Irreversible damage (necrosis) within 20 - 40 min.
- 10. MI • Transmural MIinfarction implies an infarction that resulted in necrosis of the tissue in all the layers of the myocardium (up to the epicardium) • Transmural MI infarction compromises CO as area of infarction may become dyskinetic with small infarction, or akinetic with a large infarction. • Determinants of ventricular function post MI include infarction size, location, & type ❑ Size of Infarction is determined by: o Extent, severity, & duration of ischemia o Size of the vessel; & amount of collateral circulation o Status of the intrinsic fibrinolytic system; & the metabolic demands of the myocardium.
- 11. ❑ MIs Location: ▪Anterior left ventricle o Occlusion of left anterior descending (LAD) ▪ Lateral & posterior left ventricle o Left circumflex artery ▪ Inferior left ventricle o Occlusion of right coronary artery ▪ Inferior Right ventricle o Occlusion of right coronary artery MI
- 12. Types of MIInfarction ▪ STEMI= ST-segment elevation MI • More common • Usually the affected coronary artery is completely occluded • Mostly ends up with Q wave thus causing Q-wave MI • The primary goal of initial treatment is early reperfusion therapy through administration of fibrinolytics or mechanical reperfusion.
- 13. Types of MIInfarction ❑ NSTEMI = non ST-segment elevations MI • Related to partially or intermittently occluding thrombus. • Unstable angina (UA) & NSTEMI are difficult to distinguish initially, both presented with similar symptoms & ECG changes (significant ST-segment depression & T-wave inversions) • An elevated biomarker is detected with NSTEMI but not UA • Management strategies for UA/NSTEMI include Antiplatelet, Antithrombin, & Antianginal • Fibrinolysis is contraindicated with NSTEMI & UA • An invasive strategy is indicated in patients with positive biomarkers or unstable clinical features.
- 14. Assessment/History • Chest discomfortor pain, described as heaviness, squeezing, or choking (the most common complaint) • Patients describe as “someone sitting on my chest.” • The substernal pain radiate to the neck, left arm, back, or jaw • Unlike the pain of angina, the pain of an MI is often more prolonged & unrelieved by rest or sublingual nitroglycerin • Nausea & vomiting, thus patients may initially seek relief of the gastrointestinal symptoms through antacids & other home remedies. • Diaphoresis, dyspnea, weakness, fatigue, anxiety, restlessness, confusion, shortness of breath, or a sense of impending death.
- 15. Assessment/ Physical Examination •May appear restless, agitated, in distress ▪ Cool pale moist skin & diaphoreses • VS, low-grade fever, hypertension, & tachycardia or hypotension & bradycardia • Labored & rapid breathing, crackles • Diminished heart sounds, murmurs, pericardial friction rub • JVD, heart failure, pulmonary edema
- 16. Diagnostic Tests/ECG ▪ AnECG can be used to detect patterns of ischemia, injury, & infarction • Ischemia—T-wave inversion, ST-segment depression • Injury—ST-segment elevation • Infarction—T-wave, ST-segment, & Q-wave changes • Myocardial ischemia is caused by 70% occluded coronary artery with & oxygen demand exceeding oxygen supply • uncorrected ischemic state leads to injury • uncorrected injury leads to MI • Ischemia & injury are reversible but infarction is irreversible.
- 17. Effects of Ischemia,Injury, Infarction on ECG • Involve changes in the T wave, the ST segment, & the Q wave in the leads overlying the infarcted area.
- 18. ECG Changes inAMI/Infarction ▪ Stage 1: Hyperacute or peaked T waves phase: • T waves become tall & narrow, after a few hours, these hyperacute T waves invert
- 19. ECG Changes duringAMI • Hyperacute T waves may precede ST segment elevation (A) or seen at the same time with ST elevation (B) during this acute phase.
- 20. ECG Changes inAMI/Infarction ▪ Stage 2: the ST segments elevate from several hours to several days in the leads of the ECG facing the infracted heart. • In the normal ECG, the ST segment should not be elevated more than 1 mm in the standard leads or more than 2 mm in the precordial leads. • The leads facing away from the injured area may show ST segment depression (reciprocal changes), most likely to be seen at the onset of infarction & disappear later
- 21. ECG Changes inAMI/Infarction ▪ Stage 3: development of Q waves • Q waves compatible with an MI are usually 0.04 second or more in width or one-fourth to one-third the height of the R wave • Small, narrow Q waves may be seen in the normal ECG in leads I, II, III, aVR, aVL, V5, & V6 • Q waves develop within the fist 24 to 48 hours after the infarction
- 22. ECG Changes duringAMI ▪ Last stage: few days after the MI • The elevated ST segments return to baseline. o Persistent elevation of the ST segment may indicate the presence of a ventricular aneurysm. • The T waves may remain inverted for several weeks, indicating areas of ischemia near the infarcted region. Eventually, the T waves should return to their upright configuration. • The Q waves do not disappear and therefore always provide ECG evidence of a previous MI. o Abnormal Q waves accompanied by ST segment elevations indicate an acute MI. o Abnormal Q waves accompanied by a normal ST segment indicate a previous MI.
- 23. ECG Changes inAMI Figure 21-8 Evolution of the electrocardiogram (ECG) in a patient with MI. A: Tall peak T waves known as hyperacute T waves. B: Symmetrical T-wave inversions. C: ST-segment elevation. D: Development of the Q wave.
- 24. The 12-lead ECG:Correlation of lead with the view of the heart
- 25. The 12-lead ECG:Correlation of lead with the view of the heart
- 27. Correlation of leadwith the view of the heart
- 28. MI Location Coronary artery ECG leadsClinical impact Anteroseptal MI most common LAD ventricular septum, anterior left ventricle & most of bundle branches. V1 –V4 Q waves and ST segment elevations Significant hemodynamic Compromise: CHF, pulmonary edema, cardiogenic shock; intraventricular conduction disturbances (e.g., RBBB, LBBB)
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- 30. Septal MI Acute septalMI is associated with ST elevation, Q wave formation and T wave inversion in the leads overlying the septal region of the heart (V1 & V2)
- 31. MI Location Coronaryartery ECG leads Clinical impact Lateral wall MI Left circumflex Perfuse the SA node in 45% of people and AV node in 10% of people I, aVL, V5, V6, Q waves, ST segment elevations Some hemodynamic Changes dysrrhythmias such as sinus arrest and junctional rhythm
- 32. Lateral wall MI Figure21-10 Twelve-lead ECG showing an acute lateral wall MI. ST-segment elevations can be seen in leads I, aVL, V5 & V6. Note also the deep Q waves in II, III, and aVF & normal ST segments, indicating a previous inferior wall MI.
- 33. Location Coronary artery ECG leads Clinicalimpact Posterior wall MI Left circumflex Perfuse the SA node in 45% of people and AV node in 10% of people V1 and V2 all upright R waves with ST segment depression (reciprocal changes) V7 - V9 (15 lead ECG) : Q waves and ST segment elevation Some hemodynamic changes; dysrrhythmias such as sinus arrest and junctional rhythm
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- 35. MI Location Coronaryartery ECG leads Clinical impact Inferior wall less common than anteroseptal more common than lateral or posterior RCA Supplies SA node in 50% of people and the AV node in 90% of people II, III, aVF Q waves and ST segment elevation Some hemodynamic changes Potential for significant arrhythmias caused by SA and AV node dysfunction
- 36. Inferior wall MI Figure21-11 ECG showing an acute inferior wall MI. Note the ST-segment elevations in II, III, and aVF. The posterior wall infarction is evidenced by a tall R wave, ST-segment depression, and inverted T wave in V1 and V2.
- 37. Types of MI LocationCoronary artery ECG leads Clinical impact Right ventricular wall 50% of patients will have also inferior MI RCA Supplies blood to the SA node in 50% of people and the AV node in 90% of people right precordial chest leads (RV1 through RV6) Q waves and ST segment elevations Some hemodynamic changes Potential for significant arrhythmias caused by SA and AV node dysfunction
- 38. Inferior and RVMI Right ventricular infarction. The six chest leads have been positioned on the right side of the chest. Note the ST segment elevation in RV4, RV5, & RV6. ST segments in the inferior leads (II, III, aVF) indicating inferior wall MI Figure 21-13 Twelve-lead ECG showing right ventricular infarction. The six chest leads have been positioned on the right side of the chest. Note the ST-segment elevation in RV4, RV5, and RV6. The ECG also shows elevated ST segments in the inferior leads (II, III, aVF). Patients with an inferior wall MI often also have an infarction in the right ventricle.
- 39. Diagnostic tests/ Labtests • Cardiac Troponins – Preferred biomarker – Are proteins with two subforms (troponin T & troponin I,) that are highly specific for cardiac muscle. (Troponin C which is not sensitive to MI) – Troponin levels are not detected in the healthy person & not affected by skeletal muscle injury. – Troponin I levels rise in about 3 to 12 hours, peak at 24 hours & remain elevated for 5 to 10 days. – Troponin T levels rise in 3 to 12 hours, peaks in 12 hours- 2 days & remains elevated for 5 to 14 days. – Excellent diagnostic markers for patients who present late with symptoms of MI.
- 40. Diagnostic tests/ Labtests ▪ Creatine Kinase (CK) • CK is an enzyme found mainly in heart & skeletal muscles. When heart muscle is damaged, CK is released into the blood. • Onset 6 to 8 hours after the MI, peaks within 12 to 28 hours, & returns to normal in 24 to 36 hours • The isoenzyme (CK MB) offers a more definitive indication of myocardial cell damage than total CK alone. • CK-MB appears in the serum in 6 to 12 hours, peaks between 12 & 28 hours, & returns to normal levels in about 72 to 96 hours. • In the patient with an MI, the CK-MB2 level rises resulting in a CK-MB2 to CK-MB1 ratio greater than one
- 41. Diagnostic tests/ Labtests • Myoglobin – Myoglobin is an oxygen-binding protein found in skeletal & cardiac muscle (thus it is not specific to the heart) – Onset within 1 to 2 hours of acute MI & peaks within 3 to 15 hours – The early release of myoglobin makes it valuable in helping to detect MI
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- 43. Management ▪ Early management •An initial evaluation (Hx, PE, ECG, monitor) of the patient should occur ideally within the first 10 minute • Continuous cardiac monitoring & Serial ECGs required • Administer Aspirin, 160 to 325 mg chewed, to diminishes platelet aggregation • Give oxygen by nasal cannula , use pulse oximeter, & draw ABG. o hypoxemia often occurs in patients with a myocardial infarction because of pulmonary edema. o If severe pulmonary edema is present & the patient is in respiratory distress, intubation may be necessary o Serum cardiac markers, CBC, chemistry, and lipid profile
- 44. Management • Administer sublingualNitroglycerin (unless the systolic BP is less than 90 mm Hg or the heart rate is less than 50 or greater than 100 beats/minute) • Nitroglycerin promotes vasodilation but is relatively ineffective in relieving pain in the early stages of a MI. • Intravenous nitroglycerin is recommended for the first 24 to 48 hours for patients with acute MI & heart failure, large anterior wall infarctions, persistent ischemia, or hypertension. • Morphine is the drug of choice to relieve the pain of a MI. o given intravenously in small doses (2–4 mg) & can be repeated every 5 minutes until the pain is relieved. o Close respiratory monitoring is indicated because morphine can depress respirations
- 45. Management ▪ Percutaneous TransluminalCoronary Angioplasty (PTCA) • It is the RECOMMENDED method of reperfusion • PTCA is an invasive procedure in which the infarct- related coronary artery is dilated with a balloon catheter and possibly stent placement after balloon dilatation • PTCA is used for patients who present within 12 hours of the onset of symptoms, with persistent ischemic symptoms, OR for patients ineligible for thrombolytic therapy • A dose of 162 to 325 mg of Aspirin is given to the patient before the primary PCI and the aspirin is continued indefinitely • Complications include retroperitoneal or vascular hemorrhage, early acute reocclusion, & late restenosis
- 46. Management • Fibrinolytic therapy –Lyse coronary thrombi by converting plasminogen to plasmin which degrade fibrin and fibrinogen – The ideal door to drug time for these patients is 30 minutes. Once the patient is stabilized, the patient is evaluated for transfer to a hospital for angiography and revascularization within 3 to 24 hours. – Thrombolytic therapy provides maximal benefit if given within the first 3 hours after the onset of symptoms. – Significant benefit still occurs if therapy is given up to 12 hours after the onset of symptoms, if PCI can not be performed within 120 minutes – Fibrinolytic therapy also is recommended for patients with STEMI who are unable to receive PCI if there is clinical and/or electrocardiographic evidence of ongoing ischemia within 12 to 24 hours of symptom onset and a large area of myocardium is at risk or hemodynamically unstable
- 47. Management • The patientis closely monitored during and after the infusion of a thrombolytic agent • The nurse assesses the patient for resolution of chest pain, normalization of elevated ST segments, development of reperfusion dysrhythmias (accelerated idioventricular rhythm, ventricular tachycardia, and AV heart block) any allergic reactions, evidence of bleeding, and the onset of hypotension • The nurse monitor the development of complications such as reocclusion of the coronary artery (chest pain, ST segment elevation, and hemodynamic instability), bleeding (urine and stool for blood or altered levels of consciousness due to intracranial bleeding)
- 48. Absolute Contraindications toFibrinolytic Therapy • Previous intracranial hemorrhage or cerebrovascular events within 1 year • Known malignant intracranial neoplasm (primary or metastatic) • Known structural cerebral vascular lesion (e.g., arteriovenous malformation) • Active bleeding or bleeding diathesis (excluding menses) • Suspected aortic dissection • Significant closed-head or facial trauma within 3 months • Intracranial or intraspinal surgery within 2 months • For streptokinase/anistreplase: prior treatment within the previous 6 months or prior allergic reaction
- 49. • Severe uncontrolledhypertension on presentation (blood pressure >180/110 mm Hg) • History of prior ischemic stroke greater than 3 months • Known intracranial pathology not covered in contraindications • Current use of anticoagulants in therapeutic doses (international normalized ratio [INR] ≥2:3); known bleeding diathesis • Recent (within 2–4 weeks) internal bleeding • Head trauma or traumatic or prolonged (>10 minutes) • (CPR) or major surgery (<3 weeks) • Pregnancy/ Dementia/ Active peptic ulcer Relative Contraindications to Fibrinolytic Therapy
- 50. Management/ Pharmacological therapy ▪For management of dysrhythmias o Easy access to atropine, lidocaine, amiodarone, transcutaneous pacing patches, transvenous pacing wires, a defibrillator, & epinephrine is essential o Prophylactic Antidysrhythmics during the first 24 hours of hospitalization are NOT recommended • IV Nitroglycerin is continued for 24 to 48 hours • IV beta blocker therapy should be administered within the initial hours of the evolving infarction, followed by oral therapy (they reduce oxygen demand by decreasing the heart rate and contractility)
- 51. Management/ Pharmacological therapy •β Blockers & ACE inhibitors are initiated in the first 24 hours unless contraindicated. • β Blockers are continued during & after hospitalization • Angiotensin-converting enzyme (ACE) inhibitors are administered to patients with anterior wall MI and to patients who have an MI with heart failure in the absence of significant hypotension (they prevent ventricular remodeling (dilation) & preserve ejection fraction) • Calcium channel blockers may be given to patients in whom beta blocker therapy is ineffective or contraindicated
- 52. Management/ Pharmacological therapy •Heparin (IV or low molecular weight) is given to patients MI because of the high risk of embolism • Daily aspirin is continued on an indefinite basis. • Clopidogrel is added to the aspirin regimen for patients with an STEMI and is continued for 14 days. • Thrombotic thrombocytopenic purpura is associated with the prolonged use of Clopidogrel • During the first several days after STEMI, it is important to normalize the patient’s blood glucose levels. – An insulin infusion may be required to achieve this goal. • Lipid management therapy is initiated if indicated.
- 53. Management ▪ Other interventions •Hemodynamic monitoring – Use of a pulmonary artery catheter (check volume status, CO) . – Invasive arterial monitoring is indicated
- 54. Complications ▪ Ventricular dysrhythmiasthat occur in the prehospital phase cause the majority of sudden cardiac deaths. ▪ Recurrent myocardial ischemia • Efforts are made to lower myocardial oxygen demand, to relieve pain. Emergent PTCA or surgical revascularization may be considered ▪ Cardiogenic shock • Is the most serious myocardial complication of MI. • Occurs because of the loss of contractile forces in the heart (necrosis involves 40% or more of the left ventricle), • Is the most common cause of in-hospital death for patients with MI, with a mortality rate of nearly 80%.
- 55. Complications ▪ Manifestations: rapid,thready pulse, narrow pulse pressure, dyspnea, tachypnea, inspiratory crackles, distended neck veins, chest pain, cool, moist skin, oliguria, and decreased mentation. Decreased PaO2 and respiratory alkalosis, systolic BP <85 mm Hg, a mean arterial blood pressure <65 mm Hg, PAWP >18 mm Hg (should be =18). • Interventions to cardiogenic shock include oxygen supply, IV dopamine, nitroprusside with a vasopressor (to reduce lt ventricle workload), use of an intra-aortic balloon pump (IABP) • Other complications: ventricular septal wall rupture, left ventricular wall rupture, pericarditis, DVT, pulmonary embolism, ventricular dysrhythmias and conduction disturbances
- 56. Nursing DX • ChestPain related to myocardial infarction, angina • Decreased Cardiac Output: Electrical factors affecting rate, rhythm, or conduction • Decreased Cardiac Output: Mechanical factors related to preload, afterload, or left ventricular failure • Knowledge Deficit related to illness and impact on patient’s future • Anxiety, stress related to fear of illness, death, and critical care environment • Activity Intolerance related to decreased cardiac output or alterations in myocardial tissue perfusion • Risk for Ineffective Tissue Perfusion related to thrombolytic therapy impact on myocardial tissue
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