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Cardiovascular Emergencies

Cardiovascular Emergencies. LIN LING ED ， ICU SIR RUN RUN SHAW HOSPITAL. Table of contents. 1. 2. Acute coronary syndrome. Acute heart failure. 3. 4. Hypertensive emergencies. Cardiac arrhythmias. Table of contents. 1. 2. Acute coronary syndrome. Acute heart failure. 3. 4.

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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

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