Download to read offline
ACUTE-Acute Myocardial Infarction.Nursingppt
- 1. Myocardial Infarction Myocardial Infarction KhaledDajani, MD, MBA Khaled Dajani, MD, MBA Division of Cardiology Division of Cardiology
- 2. Background Background Myocardial Infarction ifthe rapid Myocardial Infarction if the rapid development of myocardial necrosis by a development of myocardial necrosis by a critical imbalance between oxygen supply critical imbalance between oxygen supply and demand to the myocardium and demand to the myocardium
- 3. Classification Classification Acute coronary syndromesinclude Acute coronary syndromes include ST-elevation MI (STEMI) ST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) Non ST-elevation MI ( NSTEMI) Unstable Angina Unstable Angina Cardiac markers in circulation indicates Cardiac markers in circulation indicates myocardial infarction and help categorize myocardial infarction and help categorize MI and is a useful adjunct to diagnosis MI and is a useful adjunct to diagnosis
- 4. Classification Classification Anatomic or morphologic Anatomicor morphologic Transmural= Full thickness Transmural= Full thickness Non-transmural= Partial thickness Non-transmural= Partial thickness ECG ECG Q wave MI Q wave MI Non Q wave MI Non Q wave MI Does not distinguish transmural from a non- Does not distinguish transmural from a non- transmural MI as determined by pathology transmural MI as determined by pathology
- 5. Prevalence Prevalence In the US,1.3 million cases of nonfatal MI In the US, 1.3 million cases of nonfatal MI were reported in 2006 were reported in 2006 Incidence of 600 per 100,000 people Incidence of 600 per 100,000 people Increase in the proportion of NSTEMI Increase in the proportion of NSTEMI compared to STEMI compared to STEMI Approximately 500,000 to 700,000 deaths Approximately 500,000 to 700,000 deaths are caused by heart disease annually in are caused by heart disease annually in the United States the United States
- 6. History History The history iscritical in making the The history is critical in making the diagnosis of MI and sometimes provide diagnosis of MI and sometimes provide only the only clues that lead to the only the only clues that lead to the diagnosis in the initial phase of diagnosis in the initial phase of presentation presentation
- 7. History History Chest Pain- anteriorprecordium tightness Chest Pain- anterior precordium tightness Pain may radiate to jaw, neck and Pain may radiate to jaw, neck and epigastrium epigastrium Dyspnea- angina equivalent, poor LV Dyspnea- angina equivalent, poor LV function function Nausea/abdominal pain with posterior MI Nausea/abdominal pain with posterior MI Anxiety Anxiety
- 8. History History Nausea with andwithout vomiting Nausea with and without vomiting Diaphoresis or sweating Diaphoresis or sweating Syncope or near syncope Syncope or near syncope Elderly present with MS changes, fatigue, Elderly present with MS changes, fatigue, syncope or weakness syncope or weakness As many as half of MI are clinically silent As many as half of MI are clinically silent
- 9. Physical Physical The physical examcan often be The physical exam can often be unremarkable unremarkable Hypertension Hypertension Hypotension Hypotension Acute valvular dysfunction may be present Acute valvular dysfunction may be present Rales Rales Neck vein distention Neck vein distention
- 10. Physical Physical Third heart soundmay be present Third heart sound may be present A fourth heart sound poor LV compliance A fourth heart sound poor LV compliance Dysrhythmias Dysrhythmias Low grade fever Low grade fever
- 11. Causes Causes Most frequent causeis rupture of an Most frequent cause is rupture of an atherosclerotic lesion within coronary wall atherosclerotic lesion within coronary wall with subsequent spasm and thrombus with subsequent spasm and thrombus formation formation Coronary artery vasospasm Coronary artery vasospasm Ventricular hypertrophy Ventricular hypertrophy Hypoxia Hypoxia Coronary artery emboli Coronary artery emboli
- 12. Causes Causes Cocaine Cocaine Arteries Arteries Coronary anomalies Coronary anomalies Aorticdissection Aortic dissection Pediatrics Kawasaki disease, Takayasu Pediatrics Kawasaki disease, Takayasu arteritis arteritis Increased afterload which increases Increased afterload which increases myocardial demand myocardial demand
- 13. Risk factors foratherosclerosis Risk factors for atherosclerosis Age Age Male gender Male gender Smoking Smoking Hypercholesterolemia and triglyceridemia Hypercholesterolemia and triglyceridemia Diabetes Mellitus Diabetes Mellitus Poorly controlled hypertension Poorly controlled hypertension Type A personality Type A personality
- 14. Risk factors foratherosclerosis Risk factors for atherosclerosis Family History Family History Sedentary lifestyle Sedentary lifestyle
- 15. Differentials Differentials Acute coronary syndrome Acutecoronary syndrome Anxiety Anxiety Aortic stenosis Aortic stenosis Asthma Asthma Cholecystitis and biliary colic Cholecystitis and biliary colic Cholethiasis Cholethiasis COPD COPD
- 16.
- 17. Mechanisms of Myocardialdamage Mechanisms of Myocardial damage The severity of an MI is dependent of three The severity of an MI is dependent of three factors factors The level of the occlusion in the coronary The level of the occlusion in the coronary The length of time of the occlusion The length of time of the occlusion The presence or absence of collateral The presence or absence of collateral circulation circulation
- 18. Cardiac Biomarkers Cardiac Biomarkers Cardiacbiomarkers are protein molecules Cardiac biomarkers are protein molecules released into the blood stream from released into the blood stream from damaged heart muscle damaged heart muscle Since ECG can be inconclusive , Since ECG can be inconclusive , biomarkers are frequently used to evaluate biomarkers are frequently used to evaluate for myocardial injury for myocardial injury These biomarkers have a characteristic These biomarkers have a characteristic rise and fall pattern rise and fall pattern
- 19. Troponin T andI Troponin T and I These isoforms are very specific for These isoforms are very specific for cardiac injury cardiac injury Preferred markers for detecting myocardial Preferred markers for detecting myocardial cell injury cell injury Rise 2-6 hours after injury Rise 2-6 hours after injury Peak in 12-16 hours Peak in 12-16 hours Stay elevated for 5-14 days Stay elevated for 5-14 days
- 20. Creatinine Kinase (CK-MB) Creatinine Kinase ( CK-MB) Creatinine Kinase is found in heart muscle Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (MB), skeletal muscle (MM), and brain (BB) (BB) Increased in over 90% of myocardial Increased in over 90% of myocardial infraction infraction However, it can be increased in muscle However, it can be increased in muscle trauma, physical exertion, post-op, trauma, physical exertion, post-op, convulsions, and other conditions convulsions, and other conditions
- 21. Creatine Kinase (MB) CreatineKinase (MB) Time sequence after myocardial infarction Time sequence after myocardial infarction Begins to rise 4-6 hours Begins to rise 4-6 hours Peaks 24 hours Peaks 24 hours returns to normal in 2 days returns to normal in 2 days MB2 released from heart muscle and MB2 released from heart muscle and converted to MB1. converted to MB1. A level of MB2 > or = 1 and a ratio of A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury MB2/MB1 > 1.5 indicates myocardial injury
- 22. Myoglobin Myoglobin Damage to skeletalor cardiac muscle Damage to skeletal or cardiac muscle release myoglobin into circulation release myoglobin into circulation Time sequence after infarction Time sequence after infarction Rises fast 2hours Rises fast 2hours Peaks at 6-8 hours Peaks at 6-8 hours Returns to normal in 20-36 hours Returns to normal in 20-36 hours Have false positives with skeletal muscle Have false positives with skeletal muscle injury and renal failure injury and renal failure
- 23. Renal Failure andRenal Renal Failure and Renal Transplantation Transplantation Diagnostic accuracy of serum markers of Diagnostic accuracy of serum markers of cardiac injury are altered in patients with cardiac injury are altered in patients with renal failure renal failure Cardiac troponins decreased diagnostic Cardiac troponins decreased diagnostic sensitivity and specificity in patients sensitivity and specificity in patients receiving renal replacement therapy receiving renal replacement therapy Current data show levels of troponin I are Current data show levels of troponin I are unaltered while levels of troponin T may unaltered while levels of troponin T may be elevated be elevated
- 24. CBC CBC CBC is indicatedif anemia is suspected as CBC is indicated if anemia is suspected as precipitant precipitant Leukocytosis may be observed within Leukocytosis may be observed within several hours after myocardial injury and several hours after myocardial injury and returns returns to levels within the returns returns to levels within the reference range within one week reference range within one week
- 25. Chemistry Profile Chemistry Profile Potassiumand magnesium levels should Potassium and magnesium levels should be monitored and corrected be monitored and corrected Creatinine levels must be considered Creatinine levels must be considered before using contrast dye for coronary before using contrast dye for coronary angiography and percutanous angiography and percutanous revascularization revascularization
- 26. C-reactive Protein (CRP) C-reactiveProtein (CRP) C- reactive protein is a marker of acute C- reactive protein is a marker of acute inflammation inflammation Patients without evidence of myocardial Patients without evidence of myocardial necrosis but with elevated CRP are at necrosis but with elevated CRP are at increased risk of an event increased risk of an event
- 27. Chest X-Ray Chest X-Ray Chestradiography may provide clues to Chest radiography may provide clues to an alternative diagnosis ( aortic dissection an alternative diagnosis ( aortic dissection or pneumothorax) or pneumothorax) Chest radiography also reveals Chest radiography also reveals complications of myocardial infarction complications of myocardial infarction such as heart failure such as heart failure
- 28. Echocardiography Echocardiography Use 2-dimentional andM mode Use 2-dimentional and M mode echocardiography when evaluating overall echocardiography when evaluating overall ventricular function and wall motion ventricular function and wall motion abnormalities abnormalities Echocardiography can also identify Echocardiography can also identify complications of MI ( eg. Valvular or complications of MI ( eg. Valvular or pericardial effusion, VSD) pericardial effusion, VSD)
- 29. Electrocardiogram Electrocardiogram A normal ECGdoes not exclude ACS A normal ECG does not exclude ACS High probability include ST segment High probability include ST segment elevation in two contiguous leads or elevation in two contiguous leads or presence of q waves presence of q waves Intermediate probability ST depression Intermediate probability ST depression T wave inversions are less specific T wave inversions are less specific
- 30. Localization of MI Localizationof MI ST elevation only ST elevation only Inferior wall- II, III, aVF Inferior wall- II, III, aVF Lateral wall_ I, aVL, V4-V6 Lateral wall_ I, aVL, V4-V6 Anteroseptal- V1-V3 Anteroseptal- V1-V3 Anterolateral- V1-V6 Anterolateral- V1-V6 Right ventricular- RV4, RV5 Right ventricular- RV4, RV5 Posterior- R/S ratio >1 in V1 and T wave Posterior- R/S ratio >1 in V1 and T wave inversion inversion
- 31. Therapy Therapy The goals oftherapy in AMI The goals of therapy in AMI are the expedient restoration are the expedient restoration of normal coronary flow and of normal coronary flow and the maximum salvage of the maximum salvage of functional myocardium functional myocardium
- 32. Antiplatelet Agents Antiplatelet Agents Aspirinat lease 160mg immediately Aspirin at lease 160mg immediately Interferes with function of cyclooxygenase Interferes with function of cyclooxygenase and inhibits the formation of thromboxane and inhibits the formation of thromboxane ASA alone has one of the greatest impact ASA alone has one of the greatest impact on the reduction of MI mortality. on the reduction of MI mortality. Clopidogrel, ticlopidine, have not been Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior shown in any large scal trail to be superior to Aspirin in acute MI to Aspirin in acute MI
- 33. Supplemental Oxygen Supplemental Oxygen BecauseMI impairs the circulatory Because MI impairs the circulatory function of the heart, oxygen extraction by function of the heart, oxygen extraction by the heart and other tissues may be the heart and other tissues may be diminished diminished Supplemental oxygen should be Supplemental oxygen should be administered to patient with symptoms and administered to patient with symptoms and or signs of pulmonary edema or pulse or signs of pulmonary edema or pulse oximetry readings less than 90%. oximetry readings less than 90%.
- 34. Nitrates Nitrates IV nitrates toall patients with MI and IV nitrates to all patients with MI and congestive heart failure, persistent congestive heart failure, persistent ischemia, hypertension, or large anterior ischemia, hypertension, or large anterior wall MI wall MI Primary benefit vasodilator effect Primary benefit vasodilator effect Metabolized to nitric oxide in the vascular Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium endothelium, relaxes endothelium Vasodilatation reduces myocardial oxygen Vasodilatation reduces myocardial oxygen demand and preload and afterload demand and preload and afterload
- 35. Beta-blockers Beta-blockers Recommended within 12hours of MI Recommended within 12 hours of MI symptoms and continued indefinitely symptoms and continued indefinitely Reduces Myocardial mortality by Reduces Myocardial mortality by decreasing arrythmogenic death decreasing arrythmogenic death Decrease the rate and force of myocardial Decrease the rate and force of myocardial contraction and decreases overall oxygen contraction and decreases overall oxygen demand demand
- 36. Unfractionated heparin Unfractionated heparin Formsa chemical complex with Forms a chemical complex with antithrombin III inactivates both free antithrombin III inactivates both free thrombin and factor Xa thrombin and factor Xa Recommended in patients with MI who Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with undergo PTCA or fibrinolytic therapy with alteplase alteplase
- 37. Low-molecular weight heparin Low-molecularweight heparin Direct activity against factors Xa and IIa Direct activity against factors Xa and IIa Proven to be effective in treating ACS that Proven to be effective in treating ACS that are characterized by unstable angina or are characterized by unstable angina or non ST- elevation MI non ST- elevation MI Their fixed doses are easy to administer Their fixed doses are easy to administer and laboratory testing to measure their and laboratory testing to measure their therapeutic effect is not necessary makes therapeutic effect is not necessary makes them attractive alternative of un- them attractive alternative of un- fractionated heparin fractionated heparin
- 38. Thrombolytics Thrombolytics Indicated with MIand ST segment Indicated with MI and ST segment elevation greater than 0.1mV in 2 elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset contiguous ECG leads, or new onset LBBB, who present less than 12 hours but LBBB, who present less than 12 hours but not more than 24 hours after symptom not more than 24 hours after symptom onset onset The most critical variable in achieving The most critical variable in achieving successful fibrinolysis is time form successful fibrinolysis is time form symptom onset to drug administration symptom onset to drug administration
- 39. Thrombolytics Thrombolytics As a classthe plasminogen activators have As a class the plasminogen activators have been shown to restore coronary blood flow in 50- been shown to restore coronary blood flow in 50- 80% of patients 80% of patients Contraindication active intracranial bleeding, Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, CVA 2months, CNS neoplasm, HTN, coagulopathy coagulopathy Retaplase slightly higher angiographic patency Retaplase slightly higher angiographic patency but did not translate into survival benefit but did not translate into survival benefit Intracranial bleed risk major drawback Intracranial bleed risk major drawback
- 40. Glycoprotein IIb/IIIa Antagonists GlycoproteinIIb/IIIa Antagonists Potent inhibitors of platelet aggregation Potent inhibitors of platelet aggregation Use during PCI and in patients with high Use during PCI and in patients with high risk features ACS have been shown to risk features ACS have been shown to reduce the composite end points of death, reduce the composite end points of death, reinfraction and the need for target lesion reinfraction and the need for target lesion
- 41. Percutanous Coronary Intervention PercutanousCoronary Intervention Alternative if performed by skilled operator Alternative if performed by skilled operator in an experienced center in an experienced center Standard is a “ door to balloon” time of 90 Standard is a “ door to balloon” time of 90 minutes minutes PCI can successfully restore coronary PCI can successfully restore coronary blood flow in 90 to 95% of MI patients blood flow in 90 to 95% of MI patients PCI definitive survival advantage over PCI definitive survival advantage over fibrinolytics for MI patients who are in fibrinolytics for MI patients who are in cardiogenic shock cardiogenic shock
- 42. Surgical Revascularization Surgical Revascularization Emergentor surgical revascularization in Emergent or surgical revascularization in setting of failed PTCA in patients with setting of failed PTCA in patients with hemodynamic instability and coronary hemodynamic instability and coronary anatomy amendable to surgical grafting anatomy amendable to surgical grafting Also indicated of mechanical Also indicated of mechanical complications of MI including VSD, free complications of MI including VSD, free wall rupture, or acute MR wall rupture, or acute MR Carries a higher risk of perioperative Carries a higher risk of perioperative mortality than elective CABG mortality than elective CABG
- 43. Lipid Management Lipid Management Allpost MI patients should be on AMA All post MI patients should be on AMA step II diet ( < 7% of calories from step II diet ( < 7% of calories from saturated fats) saturated fats) Post MI patients with LDL > 100 mg/dl are Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try recommended to be on drug therapy to try to lower levels to <100 mg/dl to lower levels to <100 mg/dl Recent data indicate that all MI patients Recent data indicate that all MI patients should be on statin therapy, regardless of should be on statin therapy, regardless of lipid levels or diet lipid levels or diet
- 44. Long term Medications Longterm Medications Most oral medications instituted in the Most oral medications instituted in the hospital at the time of MI are continued hospital at the time of MI are continued long term long term Aspirin, beta blockers and statin are Aspirin, beta blockers and statin are continued indefinitely continued indefinitely ACEI indefinitely in patients with CHF, ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or ejection fraction <.40, hypertension, or diabetes diabetes
- 45.