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1、ACUTE CORONARY SYNDROMES: Acute MI and Unstable AnginaTintinalli Chapter 50September 20, 2005Acute Coronary Syndrome (ACS)nIschemic heart disease accounts for 500,000 deaths annually in the U.S.nCAD and myocardial ischemia contribute to 5 million ER visits yearly for chest painn15% of pts with chest
2、 pain will have acute MI and 25-30% will have unstable anginaACSna term used to describe pts with acute CP and other symptoms of myocardial ischemianDuring the initial exam, often not possible to determine whether permanent damage to the myocardium has occurredOnly in retrospect after serial ECGs or
3、 cardiac markers can the distinction b/w AMI or UA be madePathophysiologynACS is caused by secondary reduction in myocardial blood flow due to coronary arterial spasmdisruption of atherosclerotic plaquesplatelet aggregation or thrombus formation at site of atherosclerotic lesionThrombus formationnAt
4、herosclerotic plaque formation occurs through repetitive injury to vessel wallnWhen plaque ruptures, potent thrombogenic substances are exposed to plateletsnThese platelets respond by adhesion, activation, and aggregation thus initiating thrombus formation in the coronary vesselsnThe extent of O2 de
5、privation and thus clinical presentation of ACS depend on the limitation of O2 delivery by thrombus adhering to fixed, fissured, or eroded plaquesStable AnginanIschemia occurs only when activity induces O2 demands beyond the supply restrictions imposed by a partially occluded coronary vesselnoccurs
6、at a relatively fixed and predictable point and changes slowly over timenatherosclerotic plaque has not ruptured thus there is little superimposed thrombusACS nAtherosclerotic plaque rupture and platelet-rich thrombus developnDegree and duration of O2 supply-demand mismatch determines whether revers
7、ible myocardial ischemia w/o necrosis (unstable angina) or myocardial ischemia w/ necrosis (myocardial infarction) Clinical FeaturesnMain symptom of ischemic heart disease is chest painneed to characterize its severity, location, radiation, duration, and qualityask about associated symptoms: N/V, di
8、aphoresis, dyspnea, lightheadedness, syncope, palpitationsnReproducible chest wall tenderness is not uncommonnPatients with ACS may complain of easy fatigabilitynUsually an AMI is accompanied by more prolonged and severe chest discomfort and more prominent associated symptomsAngina PectorisnExercise
9、, stress, or cold environment classically precipitates anginanduration of symptoms typically nAnterior -nanterolateral -nQS deflections in V1-V3, possibly V4nrS defection in V1, Q waves V2-4 or decr in amplitude of initial R wave in V1-V4nQ waves in V4-6, I, aVLECG Criteria and AMInLateral -ninferio
10、r -ninferolateral -ntrue posterior -nright ventricular -nQ waves in I, aVLnQ waves II, III, aVFnQ waves II, III, aVF, and V5-V6nInitial R waves in V1-V2 0,04s and R/S ratio 1nQ waves II, III, aVF & ST elevation rV4ECGnIn distributions previously described:ST elevation suggests acute transmural injur
11、yST depression suggests subendocardial ischemianAll inferior wall MI should have right sided ECGST elevation in rV4 indicates right ventricular infarctionECGnReciprocal ST segment changes predict: a larger infarct distributionan increased severity of underlying CADmore severe pump failurea higher li
12、kelihood of cardiovascular complicationsincreased mortalityDifficult ECG interpretationsnST elevation in absence of AMIearly repolarizationLVHpericarditis/myocarditisLeft ventricular aneurysmHypertropic cardiomyopathyhypothermiaventricular paced rhythmsLBBBDifficult ECG interpretationsnST depression
13、 in absence of ischemiahypokalemiadigoxin effectcor pulmonale and right heart strainearly repolarization LVHventricular paced rhythmsLBBBDifficult ECG interpretationsnT wave inversions without ischemiapersistent juvenile patternseizures or Stokes Adams syncopepost-tachycardia T wave inversionpost-pa
14、cemaker T wave inversionIntracranial pathology (CNS hemorrhage)Mitral valve prolapsepericarditisprimary or secondary myocardial diseasenT wave inversion without ischemiaPE or cor pulmonalespontaneous PTXmyocardial contusionLVHventricular paced rhythmsRBBBLBBBAMI and LBBBnIn the setting of LBBB, the
15、following are indicative of AMI1. ST elevation 1mm or greater and concordant with the QRS complex2. ST depression 1mm or more in leads V1, V2, or V33. ST elevation 5mm or greater and discordant with the QRS complexCardiac EnzymesnSerial measurements are more sensitive and accurate than initial singl
16、e measurementnserum markers have less utility in the diagnosis of UA, only about 50% will have elevated troponinsCK-MBnMost commonly used marker in ACSna serial rise to above 5 times baseline followed by fall back to baseline is considered diagnostic for AMInpeaks at 12-24 hours, with fall back to b
17、aseline in 2-3 daysnuseful in detecting recurrent infarction after the initial 24-48 hours by noting a repeat elevation in the levelConditions Associated with Elevated CK-MBnUnstable anginanacute coronary ischemianinflammatory heart diseasencardiomyopathiesncirculatory failure & shocknDTsnRhabdomyol
18、ysisnCardiac surgerynskeletal m. traumandermatomyositis, polymyositisnmyopathic disordersnmuscular dystrophynvigorous exercisenmalignant hyperthermianEthanol poisoning (chronic)TroponinnMain regulatory protein for the actin-myosin myofibrilsn3 subunits: inhibitory subunit (Trop I)tropomyosin binding
19、 subunit (Trop T)calcium binding subunit (Trop C)nTrop I has not been identified in skeletal m. during any stage of develop therefore specific to myocardium TroponinnPeak level in 12 hoursnprolonged elevation for 7 to 10 days before returning to baselinethus making trop of no use in detecting recurr
20、ent infarctions during this timenRise in serum Trop I or T is considered diagnostic for AMInLow level elevations in Trop correlate with risk for CV complications in UA, CAD, and renal failureMyoglobinnRises within 2-3 hours of symptoms onsetnpeaks within 4 to 24 hoursnmore sensitive than CK and CK-M
21、B but not specific for cardiac musclenthere is a high false-positive rate due to its presence in all muscle tissueComplications of MIn1. Dysrhythmias and conduction disturbancesn2. Cardiac failuren3. Mechanical complicationsn4. Pericarditisn5. Right Ventricular Infarctionn6. OtherDysrhythmiasnOccurs
22、 in 72-100% of AMI pts treated in coronary care unitnPVCs are common in AMIoccur in 90% of AMI patientsnAtrial premature contractions are also commonoccur in up to 50% of AMI patientsnot associated with increased mortalityDysrhythmiasnEarly in AMI, pts often show increased autonomic nervous system a
23、ctivitysinus brady, AV block, hypotension occur from increased vagal tonenLater, increased sympathetic activity results in incr catecholamine release thus creates electrical instability: PVCs, Vtach, Vfib, accelerated idioventricular rhythms, AV junctional tachycardiaDysrhythmiasnHemodynamic consequ
24、ences of dysrhythmias are dependent on ventricular functionNormal hearts have a loss of 10-20% of left ventricular output when atrial kick is eliminatedReduced left ventricular compliance can result in 35% reduction in stroke volume when the atrial systole is eliminatedDysrhythmiasnPersistant tachyc
25、ardia is associated with poor prognosisdue increase myocardial oxygen usenWhen Vtach occurs late in AMI course, usually associated with transmural infarct and left ventricular dysfunctioninduces hemodynamic deteriorationmortality rate approaches 50%Conduction DisturbancesnFirst degree and Mobitz I (
26、Wenckebach)more common with inferior AMIintermittent during the first 72 hrs after infarctionrarely progresses to complete block or pathologic rhythmnMobitz II usually associated with anterior AMIdoes progress to complete heart blockConduction DisturbancesnComplete Heart Blockoccurs in setting of in
27、ferior MIusually progresses from less AV blocksthis form is usually stable & should resolveMortality is 15% in absence of RV involvement & increases to 30% when RV is affectednComplete block in setting of anterior MI results in grave prognosisConduction DisturbancenNew RBBBoccurs in approximately 2%
28、 of AMI ptsassociated with anteroseptal AMIassociated with increased mortality because often leads to complete AV blockConduction DisturbancenNew LBBBoccurs in 5% of pts with AMI associated with high mortalityLeft posterior hemiblock associated with higher mortality than isolated anterior hemiblockr
29、epresents larger area of infarctionCardiac Failuren15-20% of AMI pts present in some degree of CHFnMore severe the degree of left ventricular dysfunction, the higher the mortalitydependent on the net effect of prior myocardial dysfunction, baseline myocardial hypertrophy, acute myocardial necrosis,
30、& acute reversible dysfunction (“stunned myocardium”)Cardiac FailurenB-type natriuretic peptideuseful for risk stratification of pts with non ST elevation MI and UAelevated levels of BNP early in the hospital course predict a worse outcome at 30 daysMechanical Complicationsof AMInSudden decompensati
31、on of previously stable AMI pt should raise concern of the “mechanical” complication nFree wall ruptureoccurs in 10% of AMI fatalities, usually 1 to 5 days after infarctionrupture of LV free wall usually leads to pericardial tamponade and death (90% of cases)Mechanical Complicationsof AMInNSAIDs, st
32、eroids, and late administration of thrombolytics have been linked to an increased likelihood of cardiac rupturehowever, studies remain contradictorynLV hypertrophy appears to be protectiveMechanical Complicationsof AMInRupture of interventricular septumis more often detected clinically than ventricu
33、lar wall rupturepts have chest pain, dyspnea, sudden appearance of new holosystolic murmurmurmur often associated with palpable thrill and best heard at lower left sternal bordermore common in pts with anterior wall MI and pts with extensive (3 vessel) CADMechanical Complicationsof AMInPapillary Mus
34、cle Ruptureoccurs in 1% of pts with AMImore common with inferior wall MIusually occurs 3 to 5 days after AMIoccurs with a small to modest sized MIposteromedial m. commonly rupturedreceives blood from only one coronary a.present with acute dyspnea, increasing CHF, and new holosystolic murmur consiste
35、nt with mitral regurgitationPericarditisnOccurs in 10-20% of post-AMI ptsnmore common with transmural MInusually occurs 2-4 days after AMInPericardial friction rubs detected more often with inferior wall and right ventricular infarctsnPericardial effusions may also be present; may take months to res
36、orbnDressler Syndromepost AMI syndromeoccurs 2 to 10 weeks after AMIpts presents with chest pain, fever, and pleuropericarditisRight Ventricular InfarctionnUsually seen as a complication of an inferior infarctionapproximately 30% of inferior wall MI involve the RVnPresence of RV infarction is associ
37、ated with significant increase in mortality and cardiovascular complicationsOther ComplicationsnLeft ventricular thrombus formationnarterial embolization nvenous thrombusnpulmonary embolismnpostinfarction anginaninfarct extension*these are diagnoses to think about when a pt presents to the ER after
38、recent discharge from the hospitalPostprocedure Chest PainnPts who present with symptoms of ACS shortly after angioplasty or stent placement should be assumed to have abrupt vessel closurenSubacute thrombotic occlusion after stent placement occurs in approximately 4% of pts 2 to 14 days after proced
39、urethis less common than closure after angioplastynPts with chest pain syndromes after CABGmay have abrupt vessel closuresymptoms of recurrent ischemia can be confused with post-AMI pericarditisDispositionnAll patients with acute chest pain need to be evaluated for the possibility of ACSpts are admi
40、tted to appropriate level of care depending on their risksnResults of prior cardiac catheterization are very useful for risk stratificationCardiac Cath Resultspts with previously documented minimal stenosis (25%) or normal coronary arteriograms have excellent long-term prognosismore than 90% of thes
41、e pts are free from MI 10 yrs latera recent cardiac cath (within last 2 yrs) with normal or minimally diseased vessels almost eliminates the possibility of ACS due to atherosclerosisdoesnt eliminate vasospasm or small vessel dzStress Tests ResultsnWhen pts complete all stages of the stess protocol,
42、have no ECG changes and normal imaging studies, exercise testing can r/o acute ischemic syndromes with sensitivities b/w 80-90%nIf all criteria are not met, stress test have poor sensitivityQUESTIONS?n1. Which of the following is false about new RBBB?a. Occurs in 2% of AMI ptsb. Occurs most commonly
43、 with inferior wall MIc. Often leads to complete AV blockd. Associated with increased mortalityQUESTIONS?n2. True or False: Inferior wall MI can result from occlusion of left circumflex a. or RCAn3. True or False: Left ventricular free wall rupture occurs in 10% of AMI fatalities usually 3-4 weeks a
44、fter initial infarctQUESTIONS?n4. True or False: B type natriuretic peptide has a high specificity in diagnosing CHFn5. True or False: Reproducible chest wall pain rules out ACS.nAnswers: B, true, false, false, falseReferencesnTintinalli, J. “Emergency Medicine: A Comprehensive Study Guide.” 6th edition. pg. 343-351.nMa, O.J. and David Cline. “Emergency Medicine: Just the facts.” 2nd edition. pg. 91-97.nRivers, C. “Preparing for the Written Board Exam in Emergency Medicine.” 4th edition. pg. 60-76.
