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Cardiovascular Emergencies

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  1. Cardiovascular Emergencies LIN LING ED,ICU SIR RUN RUN SHAW HOSPITAL

  2. Table of contents 1 2 Acute coronary syndrome Acute heart failure 3 4 Hypertensive emergencies Cardiac arrhythmias

  3. Table of contents 1 2 Acute coronary syndrome Acute heart failure 3 4 Hypertensive emergencies Cardiac arrhythmias

  4. CONCEPT • Hypertensive emergency is defined as the acute and progressive decompensation of damage of vital organ function caused by an elevated blood pressure

  5. CONCEPT • Major organs affected by hypertension are the brain,kidney, heart, and vascular system. • Need to be carefully evaluated ,be monitored, and have their blood pressure controlled. • The important issue is clinical situation,not the severity of BP level. No degree of hypertension by itself defines an emergency

  6. Hypertensive urgency • Usually referring to markedly elevated BP and without symptoms. • No longer widely used. • Can be managed on an outpatient basis. • Do require increased vigilance, the pts are at high risk of nearterm complications from their uncontrolled hypertension,especially those pts with a history of previous end-organ disease.

  7. Hypertensive emergencies • Hypertensive encephalopathy • Accelerated malignant hypertension • Cerebrovascular accidents • stroke • Cardiovascular crisis • Pulmonary edema • Heart failure • Renal crises • Other emergencies • Preeclampsia/eclampsia

  8. ED EVALUATION • A-B-C • accurate measurements of BP • History • PE • Diagnositc studies

  9. Accurate measurement of BP • Several separate BP measurements : • Initially elevated Bp frequently decrease spontaneously by a second reading • Evaluated in both arms • Seated with the arm at the level of the heart and the cuff bladder should cover at least 80%of the arm circumference Base clinical decisions on correctly measured and repeated BP

  10. history • Start with the target organ • Dyspnea,chest pain,neurologic complaints ,visual changes • Duration and severity of preexisting hypertension • The degree of previous success with BP control • The presence of target organ dz

  11. PE • Directed toward identifying signs of target organ damage • funduscopic examination • retinal hemorrhage or papilledema is sufficient to diagnose accelerated malignant hypertension • Cardiovascular • Neurologic :

  12. Diagnostic studies • Based on the pt’s symptoms • CXR • Head CT • ECG • Urine screen and Serume cratinine

  13. ED Management • The goal of therapy is a reduction in the mean MAP by 20%to 25% in 1 to 2 hrs. • NOTE:Reducing BP too quickly or too low a level.----can result in inadequate cerebral or cardiac blood flow leading to stroke or myocardial infarction.

  14. ED Management • All hypertensive emergencies require admission to a monitored setting . • Close BP monitoring ,preferably with an A-line. • Pts with preeclampsia/eclampsia require emergent obstetric consultation

  15. ED Management • Search for and correct underlying causes of an elevated BP (e.g.pain,hypoxia,bladder distension • Avoid relative hypotension or dropping BP in the absence of an indication. • Treat the BP according to specific indications.

  16. The ideal drug • Rapid onset • Rapid maximal effect • Rapid offset • Easy titrationof BP

  17. PARENTERAL DRUGS

  18. PARENTERAL DRUGS

  19. SPECIFIC TREATMENT • Hypertensive Encephalopathy • Goal is to reduce MAP by not >25% or DBP to100mmHg in the first hour. • Nitroprussid(widely used in past)is a powerful arteriloar dilator,so a rise in ICP may occur. • Labetalol,fenoldopam used more now.

  20. SPECIFIC TREATMENT • Intracerebral Hemorrhage: • CPP=MAP-ICP. • As ICP rises,MAP must rise for perfusion but this raises risk of bleeding from small arteries and arterioles. • MAP guidelines:decrease when MAP>130 or SBP>220 • Labetalol,esmolol agents of choice.

  21. SPECIFIC TREATMENT • SAH • Nimodipinedecreases vasospasm that occurs due to chemical irritation of arteries by blood.

  22. SPECIFIC TREATMENT • Acute Ischemic Stroke: • High BP can cause hemorrhagic transformation of infarct , cerebral edema.But,if CPP is low,ischemic area may enlarged. • AHA guidelines:BP be reduced only if SBP>220 or DBP>120mmHg.(unless end-organ damage is due to BP) • Labetalol,nitroprusside-agents of choice. • For thrombolysis,BP<185/110.

  23. Specific Treatment • Aortic dissection: • Immediate reduce BP !! • mainly,shear stress(change in BP with change in time) is essential to limit the extension of damage • Eliminate pain and reduce systolic BP to 100-120 or lower that permits perfusion. • Labetalol / b-blocker + nitroprusside/other vasodilators

  24. Specific Treatment • MI: • NTG,b-blockers,ACE inhibitors. • Acute LVF: • usually associated with pulmonary edema and diastolic/systolic dysfunction. • IV nitroprusside,NTG agents of choice. • Titrate until BP controlled and signs of heart failure alleviated.

  25. Specific Treatment • Renal insufficiency: • is a cause and effect of high BP. • Goal is to prevent further renal damage by maintaining adequate blood flow. • Nitroprusside effective.

  26. Common pitfalls • Dianosing a hypertensive emergency when one does not exist. -----Elevated BP with acute end organ dysfunciton. • Reducing BP too quickly or too low a level.----can lead to cerebral or cardiac ischemia • Neglecting to match the antihypertensive agent to the clinical scenario.

  27. Table of contents 1 2 Acute coronary syndrome Acute heart failure 3 4 Hypertensive emergencies Cardiac arrhythmias

  28. Acute coronary syndrome • Is a spectrum of myocaridal ischemia , which most often due to disruption of vulnerable atherosclerotic plaques, Including • UA • NSTEMI • STEMI ACC/AHA 2007

  29. PATHOPHYSIOLOGY OF ACS动脉粥样硬化斑块的破裂和腐蚀 Disruption of vulnerable plaques

  30. DIAGNOSIS • Symptoms • ST-elevation • Positive Cardiac biomarker • symptoms • STdepression or T-wave inversion • Positive Cardiac biomarker • symptoms • With or without ECG changes • No cardiac biomarkers STEMI UA NSTEMI

  31. symptoms • Ischemic chest pain/chest discomfort • Chest Pain,tightness,or heaviness,pain that radiates to neck,jaw,teeth,shoulders,back • Others • Dyspnea • Indigestion of heartburn,Nausea/Vomitting • Weakness,dizziness,or Syncope • Intypical in DM, elder and female pts

  32. Cardiac biomarkers • CKMB • Troponin • myosin

  33. Troponin • cTnT,c TnI • Highly sensitive and highly specific • Detecting cell necrosis • High specific in cardiac • Be detected 4~6hrs after the onset of symptoms, persistes up to 5 ~14ds

  34. Pre-hospital • Every pts with chest pain should initially be assumed that the pain is ischemic in origin.——ACS suspected

  35. Prehospital and ED care Ischemic chest pain • Prehospital evaluation • ABC,and Diffibralation available • Monitor,Obtain IV access,oxygen • Aspirinshould be given except for contraindication • nitroglycerin if chest pain is ongoing • Morphin if needed • 12-lead ECG

  36. Initial management ED <10min • Monitor VS,SpO2 • IV • 12-LEAD ECG • Briefly History and PE • Thrombolysis checklist • CBC,cardiac markers,electrolytes,PT PTT • Portable X ray(30min) MONA • Oxygen,SpO2>90% • ASA 162~325mg • NTG • Morphin:chest pain not relieved

  37. Chest pain suspected ACS Transferhistory,PE Cardiac marker ER 10 min 12-lead ECG ACS NON-CARDIAC DZ STABLE ANGINA RECHECK IN 10~15MIN NON-ST ELEVATIONNSTEACS ST-ELEVATOIN TroponinNORNAL STEMI TroponinELEVATION recheck in 6 hrs UA NSTEMI

  38. TIME IS MYOCARIDIUM!TIME IS LIFE! door thrombolysis symptoms Call for help PCI goal Pt education ECG ACSprotocol PCI team Prehospital care

  39. UA/NSTEMI

  40. Three principal presentation of UA

  41. 1997/2001

  42. Although in-hospital mortality of STEMI is high,1-year mortality of NSTEM is equivalent to STEMI STEMI与NSTEMI比较的1 年累积死亡率 生存率 NSTEMI STEMI 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 after ACS (mo) Courtesy A Gitt

  43. EARLY RISK STRATIFICATIONS OF UA/NSTEMI • Selection of the site of care • Coronary care unit • Step-down unit • Outpatient setting • Selection of the therapy • Invasive managemnt strategy

  44. 非ST段抬高的AMI的危险性分层 Risk stratification of UA/NSTEMI 标准不一致时以最高为准

  45. Risk stratification of UA/NSTEMI

  46. Management of NSTEMI/UA • ER management • Pharmacoligical therapy: • Anti-platelet(aspirin,clopidogrel) • anticoagulants(heparin,LMWH) • anti-ischemic nitrates、β-blockers、Ca-A、ACEI • statins

  47. NO FIBRINOLYSIS!! NO benefit of fibrinolytic therapy in UA/NSTEMI pts was clealy demonstrated.

  48. Early invasive strategy in UA/NSTEMI is indicated in • UA/NSTEMI pts who have refractory angina • Hemodynamic or electrical instability ; • High risk pts and ineffective with pharmacologic therapy