Acute mi

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Slide 1 : Acute Myocardial Infarction
Slide 2 : DEFINITION Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. Myocardial infarction occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis. Ischemia at this critical threshold level for an extended time period results in irreversible myocardial cell damage or death.1-3
Slide 3 : DEFINITION (Cntd.) Myocardial infarction can be subcategorized on the basis of anatomic, morphologic, and diagnostic clinical information. From an anatomic or morphologic standpoint, the two types of MI are transmural and nontransmural. A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s In a nontransmural MI, the area of ischemic necrosis is limited to either the endocardium or the endocardium and myocardium. The presence or absence of Q waves does not distinguish a transmural from a non-transmural MI as determined by pathology.4
Slide 4 : DEFINITION (Cntd. II) A more common clinical diagnostic classification scheme is also based on ECG findings as a means of distinguishing between two types of MI— one that is marked by ST elevation STEMI and one that is not NSTEMI The distinction between an ST-elevation MI and a non-ST-elevation MI also does not distinguish a transmural from a non-transmural MI. The presence of Q waves or ST segment elevation is associated with higher early mortality and morbidity;
Slide 5 : ACS Types
Slide 6 : PREVALENCE In general, MI can occur at any age, but its incidence rises with age. The actual incidence is dependent upon predisposing risk factors for atherosclerosis, which are discussed below. Approximately 50% of all MI's in the US occur in people younger than 65 years of age. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years
Slide 7 : DIAGNOSIS Identifying a patient who is currently experiencing a MI can be extremely straightforward, very difficult, or somewhere in between. A straightforward diagnosis of MI can usually be made in patients who have a number of atherosclerotic risk factors along with the presence of symptoms consistent with a lack of blood flow to the heart. Patients who suspect that they are having a MI usually present to an emergency department. Once a patient's clinical picture raises a suspicion of a MI, several confirmatory tests can be performed rapidly. These tests include ECG, blood testing, and echocardiography.
Slide 8 : History PRODROMAL SYMPTOMS: history remains of substantial value in establishing a diagnosis. Resembles classic angina pectoris but it occurs at rest or with less activity than usual and can therefore be classified as unstable angina. Of the patients with AMI presenting with prodromal symptoms of unstable angina, approximately one third have had symptoms from 1 to 4 weeks before hospitalization; in the remaining two thirds, symptoms predated admission by 1 week or less, with one third of these patients having had symptoms for 24 hours or less.
Slide 9 : SIGNS AND SYMPTOMS AcuteMI may have unique presentations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. An asymptomatic MI is not necessarily less severe than a symptomatic event; but patients who experience asymptomatic MI's are more likely to be diabetic. Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax Radiation of chest pain into the jaw/teeth, shoulder, arm, and/or back Associated dyspnea or shortness of breath Associated epigastric discomfort with or without nausea and vomiting Associated diaphoresis or sweating Syncope or near-syncope without other cause Impairment of cognitive function without other cause A MI may occur at any time of the day, but most appear to be clustered around the early hours of the morning and/or are associated with demanding physical activity. Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) prior to the infarct.4
Slide 10 : Nature of Pain The pain of AMI is variable in intensity; in most patients it is severe and in some instances intolerable. The pain is prolonged, usually lasting for more than 30 minutes and frequently for a number of hours. Described as constricting, crushing, oppressing, or compressing; often the patient complains of a sensation of a heavy weight or a squeezing in the chest. Although the discomfort is typically described as a choking, viselike, or heavy pain, it may also be characterized as a stabbing, knifelike, boring, or burning discomfort. The pain is usually retrosternal in location, spreading frequently to both sides of the anterior chest, with predilection for the left side. Often the pain radiates down the ulnar aspect of the left arm, producing a tingling sensation in the left wrist, hand, and fingers. Some patients note only a dull ache or numbness of the wrists in association with severe substernal or precordial discomfort. In some instances, the pain of AMI may begin in the epigastrium and simulate a variety of abdominal disorders, a fact that often causes to be misdiagnosed as “indigestion In other patients the discomfort of AMI radiates to the shoulders, upper extremities, neck, jaw, and interscapular region, again usually favoring the left side. In patients with preexisting angina pectoris, the pain of infarction usually resembles that of angina with respect to location. However, it is generally much more severe, lasts longer, and is not relieved by rest and nitroglycerin. In some patients, particularly the elderly, AMI is manifested clinically not by chest pain but rather by symptoms of left ventricular failure and chest tightness or by marked weakness or frank syncope.98a, 98b These symptoms may be accompanied by diaphoresis, nausea, and vomiting. The recognition that pain implies ischemia and not infarction heightens the importance of seeking ways to relieve the ischemia, for which the pain is a marker. This finding suggests that the clinician should not be complacent about ongoing cardiac pain under any circumstances
Slide 11 : Other symptoms Nausea and vomiting occur in more than 50 percent of patients with transmural and severe chest pain, presumably owing to activation of the vagal reflex or to stimulation of left ventricular receptors as part of the Bezold-Jarisch reflex. These symptoms occur more commonly in patients with inferior than in those with anterior . Occasionally, a patient complains of diarrhea or a violent urge to evacuate the bowels during the phase of . Other symptoms include feelings of profound weakness, dizziness, palpitations, cold perspiration, and a sense of impending doom. On occasion, symptoms arising from an episode of cerebral embolism or other systemic arterial embolism are the first signs of AMI. The aforementioned symptoms may or may not be accompanied by chest pain.
Slide 12 : Atypical presentations of AMI (1) congestive heart failure—beginning de novo or worsening of established failure; (2) classic angina pectoris without a particularly severe or prolonged attack; (3) atypical location of the pain; (4) central nervous system manifestations, resembling those of stroke, secondary to a sharp reduction in cardiac output in a patient with cerebral arteriosclerosis; (5) apprehension and nervousness; (6) sudden mania or psychosis; (7) syncope; (8) overwhelming weakness; (9)
Slide 13 : SILENT Population studies suggest that between 20 and 60 percent of nonfatal are unrecognized by the patient and are discovered only on subsequent routine ECG or postmortem examinations. Of these unrecognized infarctions, approximately half are truly silent, with the patients unable to recall any symptoms whatsoever. The other half of patients with so-called silent infarction can recall an event characterized by symptoms compatible with infarction when leading questions are posed after the ECG abnormalities are discovered. Unrecognized or silent infarction occurs more commonly in patients without antecedent angina pectoris and in patients with diabetes98a and hypertension.102
Slide 14 : Differential Diagnosis The pain of AMI may stimulate the pain of pericarditis (see Chaps. 3 and 50), which is usually associated with some pleuritic features; that is, it is aggravated by respiratory movements and coughing and often involves the shoulder, ridge of the trapezius, and neck. An important feature that distinguishes pericardial pain from ischemic discomfort is that ischemic discomfort never radiates to the trapezius ridge, The pain due to dissection of the aorta is usually localized in the center of the chest, is extremely severe and described by the patient as a “ripping” or “tearing” sensation, is at its maximal intensity shortly after onset, persists for many hours, and often radiates to the back or the lower extremities. Often one or more major arterial pulses are absent. Pain arising from the costochondral and chondrosternal articulations may be associated with localized swelling and redness; it is usually sharp and “darting” and is characterized by marked localized tenderness. Episodes of retrosternal discomfort induced by peristalsis in patients with increased esophageal stiffness and also episodes of sustained esophageal contraction can mimic the pain of AMI.100, 101
Slide 15 : Pathophysiology Mechanisms of Occlusion: Most MIs are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists long enough (20 to 40 min), irreversible myocardial cell damage and cell death will occur.
Slide 16 : Pathophysiology (Cntd.) The development of atherosclerotic plaque occurs over a period of years to decades. The initial vascular lesion leading to the development of atherosclerotic plaque is not known with certainty. The two primary characteristics of the clinically symptomatic atherosclerotic plaque are a fibromuscular cap and an underlying lipid-rich core. Plaque erosion may occur due to the actions of metalloproteases and the release of other collagenases and proteases in the plaque, which result in thinning of the overlying fibromuscular cap. Hemodynamic forces applied to the arterial segment, can lead to a disruption of the endothelium and fissuring or rupture of the fibromuscular cap. a site otherwise known as the plaque's "shoulder region."
Slide 17 : Vulnerable Plaque
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Slide 21 : Pathogenesis OF AMI
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Slide 23 : Mechanisms of Myocardial Damage: The severity of an MI is dependent on three factors: The level of the occlusion in the coronary artery, The length of time of the occlusion The presence or absence of collateral circulation The death of myocardial cells first occurs in the area of myocardium that most distal to the arterial blood supply—that is, the endocardium. As the duration of the occlusion increases, the area of myocardial cell death enlarges
Slide 24 : Risk Factors: Six primary risk factors have been identified with the development of atherosclerotic coronary artery disease and MI: hyperlipidemia, diabetes mellitus, hypertension, Smoking (Tobacco use), male gender, and family history of atherosclerotic arterial disease. The presence of any risk factor is associated with doubling the relative risk of developing atherosclerotic coronary artery disease.
Slide 25 : DIAGNOSIS(Cntd.) Electrocardiography: The first test is the ECG, which may demonstrate that a MI is in progress or has already occurred (Figure 1). Blood Tests: Blood tests can be performed to detect evidence of myocardial cell death. Living heart cells contain certain enzymes and proteins (eg, creatine phosphokinase, troponin, and myoglobin) within cell membranes associated with specialized cellular functions such as contraction. When a heart muscle dies, cellular membranes lose integrity and intracellular enzymes and proteins slowly leak into the bloodstream. These enzymes and proteins can be detected by a blood sample analysis. The concentration of enzymes in a blood sample—and more importantly, the changes in concentration found in samples taken over time—correlates with the amount of heart muscle that has died
Slide 26 : Acute MI
Slide 27 : DIAGNOSIS(Cntd.) Echocardiography: An echocardiogram may be performed in order to compare areas of the left ventricle that are contracting normally with those that are not. One of the earliest protective mechanisms of myocardial cells utilized during limited blood flow is to "turn off" the energy requiring "machinery" for contraction, this mechanism begins within minutes after normal blood flow is interrupted. The echocardiogram can be helpful in identifying which portion of the heart is affected by a MI, and which of the coronary arteries is most likely to be occluded. Unfortunately, the presence of wall motion abnormalities on the echocardiogram may be due to an acute MI or previous (old) MI or other myopathic processes. Thus, the usefulness of echocardiography in the diagnosis of MI is limited.
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Slide 32 : DIAGNOSIS(Cntd.) Normal Values of Blood Tests to Detect Myocardial Infarction Analysis Normal Range Total creatinine phosphokinase (CPK) 30-200 U/L CPK, MB fraction 0.0-8.8 ng/mL CPK, MB fraction percent of total CPK0-4% CPK, MB2 fraction< 1 U/L Troponin I 0.0-0.4 ng/mL Troponin T 0.0-0.1 ng/mL
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Slide 39 : CK-MB,TROPONINS CRP.
Slide 40 : Time is Muscle
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Slide 43 : THERAPY The goals of therapy in AMI are the expedient restoration of normal coronary blood flow and the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient's failure to quickly recognize MI symptoms and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals.
Slide 44 : CORONARY CARE UNITS
Slide 45 : General Treatment Measures ASPIRIN CONTROL OF CARDIAC PAIN Analgesics NITRATES BETA-ADRENOCEPTOR BLOCKERS OXYGEN Limitation of Infarct Size
Slide 46 : THERAPY (Cntd.) Antiplatelet Agents: Aspirin in a dose of at least 160 mg and up to 325 mg should be administered immediately on recognition of MI signs and symptoms and continued daily indefinitely.4 The nidus of an occlusive coronary thrombus is the adhesion of a small collection of activated platelets at the site of intimal disruption in an "unstable" atherosclerotic plaque. Aspirin interferes with function of the enzyme cyclo-oxygenase and inhibits the formation of thromboxane A2. Within minutes, aspirin prevents additional platelet activation and interferes with platelet Other antiplatelet agents—including clopidogrel, ticlopidine, and dipyridamole-have not been shown in any large-scale trial to be superior to aspirin in MI. These other antiplatelet agents (specifically clopidogrel) may be useful for patients who have a true allergy to aspirin and for patients with known resistance to aspirin's effects.11-13
Slide 47 : THERAPY (Cntd.) Supplemental Oxygen: There are no published studies demonstrating that oxygen therapy reduces mortality or morbidity of a MI. Nitrates: Beta-blockers: Beta-blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely. Treatment with a beta-blocker reduces MI mortality—presumably by decreasing the incidence of arrhythmogenic death. Beta blockade decreases the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. In the setting of reduced oxygen supply in MI, the reduction in oxygen demand provided by beta blockade minimizes myocardial injury and death.
Slide 48 : Selective Beta-1-blockers
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Slide 50 : Heparin: Unfractionated Heparin: Intravenous unfractionated heparin is recommended in patients with a MI who undergo percutaneous revascularization or fibrinolytic therapy with alteplase. Intravenous unfractionated heparin is also recommended in patients with a MI who receive fibrinolytic therapy with a non-selective fibrinolytic agent (urokinase, streptokinase, anistreplase) and are at increased risk for systemic emboli (prior embolic event, large or anterior wall infarction, known left ventricular thrombus, or atrial fibrillation).4
Slide 51 : Low-molecular-weight Heparin (LMWH) LMWH can be administered to MI patients not treated with fibrinolytic therapy that have no contra-indication to heparin.4 The LMWH class of drugs includes several agents that have distinctly different anticoagulant effects. These effects can be characterized by a given agent's ratio of activity against factors Xa and IIa. LMWHs have been proven to be effective in treating acute coronary syndromes that are characterized by unstable angina and non-Q-wave MI. Their fixed doses are easy to administer, and laboratory testing to measure their therapeutic effect is not necessary.
Slide 52 : Fibrinolytics: Fibrinolytic therapy is indicated for patients with a presentation compatible with MI and ST segment elevation greater than 0.1 mV in 2 contiguous EKG leads, or new onset of a bundle branch block, who present less than 12 hours but not more than 24 hours after symptom onset.4 Restoration of coronary blood flow in MI can also be accomplished pharmacologically with the use of a fibrinolytic agent.As a class, the plasminogen activators have been shown to restore coronary blood flow in 50% to 80% of MI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years A fibrinolytic is most effective when the "door-to-needle" time is 30 minutes or less
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Slide 56 : Percutaneous Coronary Intervention: Percutaneous coronary intervention is an alternative therapy to fibrinolysis if performed by a skilled operator supported by experienced personnel performed in a well-equipped catheterization laboratory.
Slide 57 : Percutaneous Coronary Intervention: The performance standard for primary percutaneous intervention as a MI therapy is a "door-to-balloon" time of 90 minutes (± 30 minutes).4 Restoration of coronary blood flow in a MI can be accomplished mechanically by percutaneous coronary intervention (PCI). Mechanical revascularization by PCI is used as a primary therapy in many well-equipped medical centers and as an alternative to fibrinolysis when fibrinolysis is not clearly indicated or contraindicated. PCI can successfully restore coronary blood flow in 90% to 95% of a MI patients PCI provides a definite survival advantage over fibrinolysis for MI patients who are in cardiogenic shock
Slide 58 : TIMI grading system: Grade 0 = complete occlusion of the infarct-related artery. Grade 1 = some penetration of the contrast material beyond the point of obstruction but without perfusion of the distal coronary bed. Grade 2 = perfusion of the entire infarct vessel into the distal bed but with delayed flow compared with a normal artery. Grade 3 = full perfusion of the infarct vessel with normal flow
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Slide 61 : Glycoprotein IIb/IIIa Antagonists: Glycoprotein IIb/IIIa receptors on platelets bind to fibrinogen in the final common pathway of platelet aggregation. Antagonists to glycoprotein IIb/IIIa receptors are potent inhibitors of platelet aggregation. The use of intravenous glycoprotein IIb/IIIa inhibitors during PCI and in patients with MI and acute coronary syndromes have been shown to reduce the composite endpoint of death, reinfarction, and the need for target-lesion revascularization at followup
Slide 62 : Surgical Revascularization: Emergent or urgent coronary artery bypass graft surgery is warranted in the setting of failed percutaneous intervention in patients with hemodynamic instability and coronary anatomy amenable to surgical grafting. Surgical revascularization is also indicated in the setting of mechanical complications of MI such as ventricular septal defect, free wall rupture, or acute mitral regurgitation.4 Restoration of coronary blood flow with emergency coronary artery bypass grafting (CABG) can limit myocardial injury and cell death if it is performed within 2 or 3 hours of symptom onset
Slide 63 : Angiotensin Converting Enzyme Inhibitors (ACEI): Oral angiotensin converting enzyme inhibitors are recommended in MI patients within the first 24 hours of symptom onset, if no contra-indications exist.4 Contra-indications to ACEI use include hypotension and declining renal function with ACEI use. The use of an ACEI 4 to 6 weeks after presentation of MI is recommended for patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes
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Slide 65 : Calcium Antagonists GLUCOSE-INSULIN-POTASSIUM.
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Slide 69 : Post MI Management Cardiac Stress Testing: Cardiac stress testing post-MI has established value in risk stratification and assessment of functional capacity Lipid Management: All post-MI patients should be on an American Heart Association Step II diet (< 200 mg cholesterol/day, < 7% of total calories from saturated fats). Post-MI patients with LDL-cholesterol levels > 100 mg/dL on a Step II diet are recommended to be on drug therapy to lower LDL-cholesterol levels < 100 mg/dL. Post-MI patients with HDL-cholesterol levels < 35 mg/dL on a Step II diet are recommended to participate in a regular exercise program and on drug therapy designed to increase HDL-cholesterol levels.4 Recent data indicate the all MI patients should be on statin therapy, regardless of lipid levels or diet Long-term Medications: Most oral medications instituted in the hospital at the time of MI will be continued long-term. Therapy with aspirin and beta-blockade is continued indefinitely in all patients. ACEI is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes.4 A lipid-lowering agent, specifically a statin, in addition to dietary modification is continued indefinitely.
Slide 70 : Post MI Management(Cntd.) Implantable Cardiac Defibrillators: The results of the multi-center automatic defibrillator implantation trial II (MADIT II) have expanded the indications for automatic implantable cardiac defibrillators (AICD) in patients post-MI. The trial demonstrated a 31% relative risk reduction in all-cause mortality with the prophylactic use of an AICD in patients post-MI with ejection fractions less than 30%. Cardiac Rehabilitation:
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Slide 79 : Arrhythmias in AMI MECHANISM OF ARRHYTHMIAS Arrhythmias occurring in patients with AMI require aggressive treatment when they impair hemodynamics; compromise myocardial viability by augmenting myocardial oxygen requirements; predispose to malignant ventricular arrhythmias, i.e., ventricular tachycardia, ventricular fibrillation, or asystole MANAGEMENT. Given the declining incidence of ventricular fibrillation in AMI seen in CCUs over the last three decades (Fig. 37–43A Fig. 37–43A ), the prior practice of prophylactic suppression of VPBs with antiarrhythmic drugs no longer is necessary and may actually be associated with an increased risk of fatal bradycardic and asystolic events Accelerated Idioventricular Rhythm Ventricular Tachycardia Lidocaine Procainamid Amiodarone Ventricular Fibrillation BRADYARRHYTHMIAS
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Slide 81 : PHYSICAL EXAMINATION GENERAL APPEARANCE Patients suffering an AMI often appear anxious and in considerable distress. An anguished facial expression is common, and—in contrast to patients with severe angina pectoris, who often lie, sit, or stand still, recognizing that all forms of activity increase the discomfort—some patients suffering an AMI may be restless and move about in an effort to find a comfortable position. They often massage or clutch their chests and frequently describe their pain with a clenched fist held against the sternum (the “Levine” sign, named after Dr. Samuel A. Levine). In patients with left ventricular failure and sympathetic stimulation, cold perspiration and skin pallor may be evident; they typically sit or are propped up in bed, gasping for breath. Between breaths, they may complain of chest discomfort or a feeling of suffocation. Cough productive of frothy, pink, or blood-streaked sputum is common HEART RATE. BLOOD PRESSURE. TEMPERATURE AND RESPIRATION. JUGULAR VENOUS PULSE. CAROTID PULSE. THE CHEST.
Slide 82 : Cardiac Examination PALPATION AUSCULTATION. Third and Fourth Heart Sounds Murmurs. Pericardial Friction Rubs. OTHER FINDINGS FUNDI. ABDOMEN EXTREMITIES NEUROPSYCHIATRIC FINDINGS
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Slide 84 : Antithrombotic Therapy EFFECT ON MORTALITY. EFFECT ON PATENCY OF INFARCT ARTERY EFFECT ON LEFT VENTRICULAR THROMBUS NEW ANTITHROMBOTIC AGENTS HIRUDIN LOW-MOLECULAR-WEIGHT HEPARINS Antiplatelet Therapy GPIIb/IIIa INHIBITION
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