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2024-10-02 04 本頁(yè)面
  

【正文】 Possible ACS Definite ACS Treatment as indicated by alternative diagnosis ACC/AHA Chronic Stable Angina Guidelines No STElevation STElevation Nondiagnostic ECG Normal initial serum cardiac biomarkers ST and/or T wave changes Ongoing pain Positive cardiac biomarkers Hemodynamic abnormalities Evaluate for reperfusion therapy ACC/AHA STEMI Guidelines Observe ≥ 12 h from symptom onset No recurrent pain。 negative followup studies Recurrent ischemic pain or positive followup studies Diagnosis of ACS confirmed Stress study to provoke ischemia Consider evaluation of LV function if ischemia is present (tests may be performed either prior to discharge or as outpatient) Negative Potential diagnoses: nonischemic disfort。 lowrisk ACS Arrangements for outpatient followup Positive Diagnosis of ACS confirmed or highly likely Admit to hospital Manage via acute ischemia pathway Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2024。50:e1–e157, Figure 2. 第七十一頁(yè),共一百一十五頁(yè)。 ST elevation myocardial infarction STEMI 第七十二頁(yè),共一百一十五頁(yè)。 ?ischemic necrosis of myocardium ?results from the prolonged myocardial ischemia ?precipitated by an occlusive coronary thrombus at the site of a preexisting atherosclerotic plaque。 ?With typical and serial ECG changes Represent the serious situation of coronary artery disease STEMI Definition 第七十四頁(yè),共一百一十五頁(yè)。 : in USA, 71‰ in male between 3584 yrs, 22‰ in female, 1 attack in about 20 second 2. mortality: ?decreased in 30% recent 10 years ?still 1/3 of the patients died ?50% of the death occured within 1 h after the onset MI ?most deathes result from ventricular fibrillation epidemiology STEMI 第七十五頁(yè),共一百一十五頁(yè)。 Cause of the decreased mortality new drug therapy ?223。blocker, ?antithrombotic LMWH ?nitrates ?ACEI ?Statins STEMI 第七十六頁(yè),共一百一十五頁(yè)。 Change of concept ?196080s: Transmural, nontransmural or subendocardium ?1980s: Q wave MI, nonQ wave MI ?1990s: STEMI, nonSTEMI STEMI 第七十七頁(yè),共一百一十五頁(yè)。 Possible mechanism of the chronic CAD to ACS 炎癥 細(xì)胞 少量平滑肌 細(xì)胞 激活的巨噬細(xì)胞 血栓 第七十八頁(yè),共一百一十五頁(yè)。 Pathology: Coronary diseases Occlusion of LAD: anterior wall MI STEMI 第七十九頁(yè),共一百一十五頁(yè)。 Pathology: myocardium myocardial necrosis ( coagulation necrosis) coronary occlusion necrotic muscle fibres dissolved granulation tissue removal of necrosis tissue collagenzation firm connective tissue scar OMI 12hr 23d 12 weeks 6- 8 weeks STEMI 第八十頁(yè),共一百一十五頁(yè)。 STEMI Pathology: myocardial diseases 第八十一頁(yè),共一百一十五頁(yè)。 Ventricular remodeling ?concept: ? the changes in LV size, shape, and thickness ? involving both the infarcted and noninfarcted segments ?Determinants: ?the size of infarction ?Ventricular loading conditions ?Infarct related artery patency STEMI 第八十二頁(yè),共一百一十五頁(yè)。 ? Infarct expansion: ? an increase in the size of the infarcted segment. ? “acute dilatation and thinning of the area of infaction not explained by additional myocardial necrosis〞 . ? . ventricular dilatation: ? shift of pressurevolume curve of LV to the right ? larger LV volume at any given diastolic pressure ? Compensatory mechanisms for maintaining stoke volume ? Associated with nonuniform repolarization of myocardium, predispose to lifethreatening ventricular arrhythmias. STEMI Ventricular remodeling 第八十三頁(yè),共一百一十五頁(yè)。 ?Systolic function: ?dyssynchrony:dissociation in the time course of contraction of adjacent segment ?hypokinesis: reduction in the extent of shortening ?akinesis: cessation of shortening ?dyskinesis: paradoxical expansion, systolic bulging ?Diastolic function: ?reduction in LV pliance: decrease in the peak rate of decline in LV pressure (dP/dt) ?rise in LV enddiastolic pressure and volume STEMI pathophysiology LV function 第八十四頁(yè),共一百一十五頁(yè)。 ?Predisposing factor: ?heavy exercise, mental stress: ?surgical procedures ?fever, tachycardia, respiratory infection, hypoxemia, hypoglycemia ?Prinzmental’s angina ?Prodromal symptoms: ?weakness, chest disfort, restlessness , ?new onset AP and accelerating AP ?Circadian periodicity ?peak incidence:612am STEMI Clinical manifestation 第八十五頁(yè),共一百一十五頁(yè)。 Symptom ?Chest pain ?severe, sometimes intolerable, ?prolonged, usually lasting for 30 mins, ?less effective of sublingual nitroglycerin, ?retrosternal in location, ?sweating, scared, and feeling of impending death ?in some patients, AMI is manifested by shock and acute LV failure, not by chest pain ( the elderly) ?alert the epigastrium pain and abdominal disorders STEMI Clinical manifestation 第八十六頁(yè),共一百一十五頁(yè)。 symptoms ?General: fever、 HR increase、 WBC ?, ESR fasting ?Gastrointestinal symptom: nausea, vomiting , ?arrhythmias: VPs、 AV block, atrial arrhythmias occurred more often in patients with HF ?Heart failure: mainly acute LV failure, may develope RV failure. ?Initial RV failure occure in patients with RV infarction, associated with hypotension ?Hypotension and shock: SBP80mmHg after pain release, ?RV infarction STEMI Clinical manifestation 第八十七頁(yè),共一百一十五頁(yè)。 Pump failure ?Classification based on clinical examination(Killip) ?Class I: no HF, rales and S3 absent; ?Class II: mild HF, rales over 50% of lung, with or without s3; ?Class III: acute pulmonary edema, rales over 50% of lung fields ?Class IV: cardiogenic shock ?Classification based on invasive hemodynamic monitoring ?Class I: Normal, PCWP pulmonary capillary wedge pressure 18. CI; ?Class II: Pulmonary congestion, PCWP 18. CI ; ?Class III: peripheral hypoperfusion, PCWP 18, CI 。 ?Class IV: pulmonary congestion and peripheral hypoperfusion, PCWP 18, CI STEMI Clinical manifest
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