Acute-Myocardial-Infarction.ppt

Acute Myocardial InfarctionDEFINITION 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.1-3DEFINITION(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(sIn 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.4DEFINITION(Cntd.II)A more common clinical diagnostic classification scheme is also based on ECG findings as a means of distinguishing between two types of MIone that is marked by ST elevation STEMIand one that is not NSTEMIThe 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;ACS TypesPREVALENCE 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 MIs 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 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 patients clinical picture raises a suspicion of a MI,several confirmatory tests can be performed rapidly.These tests include ECG,blood testing,and echocardiography.HistoryPRODROMAL 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.SIGNS AND SYMPTOMSAcuteMI 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 MIs 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.4Nature of PainThe 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“indigestionIn 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 circumstancesOther symptomsNausea 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.Atypical presentations of AMI(1)congestive heart failurebeginning 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)acute indigestion;and(10)peripheral embolization.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.102Differential DiagnosisThe 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 chestis 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.100,101PathophysiologyMechanisms 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.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 plaques shoulder region.Vulnerable PlaquePathogenesis OF AMIMechanisms 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 occlusionThe 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 supplythat is,the endocardium.As the duration of the occlusion increases,the area of myocardial cell death enlarges 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.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 sampleand more importantly,the changes in concentration found in samples taken over timecorrelates with the amount of heart muscle that has died Acute MIDIAGNOSIS(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.DIAGNOSIS(Cntd.)Normal Values of Blood Tests toDetect Myocardial InfarctionAnalysis Normal RangeTotal creatinine phosphokinase(CPK)30-200 U/L CPK,MB fraction 0.0-8.8 ng/mLCPK,MB fraction percent of total CPK0-4%CPK,MB2 fraction 1 U/LTroponin I 0.0-0.4 ng/mL Troponin T 0.0-0.1 ng/mL CK-MB,TROPONINS CRP.Time is MuscleTHERAPY 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 patients 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.General Treatment MeasuresaspirinControl of cardiac painAnalgesicsnitratesBeta-adrenoceptor blockerOxygenLimitation of Infarct SizeTHERAPY(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 agentsincluding 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 aspirins effects(阿司匹林抵抗).11-13THERAPY(Cntd.)Supplemental Oxygen:There are no published studies demonstrating that oxygen therapy reduces mortality or morbidity of a MI.Nitrates:Beta-blockers:Beta-blocker the