Mokhtar overview & acs-2012-final

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Mokhtar overview & acs-2012-final

  1. 1. M. Sherif Mokhtar, MD Professor of Cardiology,Professor of Critical Care Medicine, Cairo University
  2. 2. 1. Relief of ischemic pain.2. Assessment of the hemodynamic state and correction of abnormalities that are present.3. Initiation of Reperfusion Therapy with primary percutaneous coronary intervention (PCI) or thrombolysis4. Antithrombotic Therapy to prevent rethrombosis of an ulcerated plaque or subtotal stenosis (Antman et al., 2004; ACC/AHA task force)
  3. 3. This is then followed by the administration ofdifferent drugs that may improve the long-termprognosis: 5. Prevention of Left Ventricular Remodeling with an angiotensin converting enzyme (ACE) Inhibitor 6. Prevention of Recurrent Ischemia and life- threatening ventricular arrhythmias with Beta Blockers
  4. 4. Administration of different drugs that may improvethe long-term prognosis: 7. Cholesterol Lowering with a Statin to prevent or slow disease progression. 8. Anticoagulation in the presence of left ventricular thrombus or chronic AF.
  5. 5. 9. Long-term Therapy: in collaboration with a cardiac rehabilitation program, involves Atherothrombotic Risk Reduction including cessation of smoking, control of hypertension and diabetes, nutritional counseling, and an exercise and stress reduction program.
  6. 6. 10. Additional Therapy is based upon the identification of patients at continued ischemic risk with: • Assessment of clinical factors. • A predischarge exercise tolerance test. • Measurement of left ventricular function.
  7. 7. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  8. 8. • Begins as soon as the patient arrives in the emergency department.• Continues in the coronary care unit.• Consists Of Acute Triage And Early Risk Stratification.
  9. 9. I) Acute TriageA focused evaluation on presentation: A. Responsiveness, Airway, Breathing and Circulation: in patients in respiratory or cardiorespiratory arrest (the appropriate CPR algorithms should be followed).
  10. 10. Acute TriageB. Evidence of Systemic Hypoperfusion (cardiogenic shock complicating acute MI requires aggressive evaluation and management).
  11. 11. Acute TriageC. Sustained Ventricular Tachyarrhythmias in the periinfarction period must be treated immediately: • Deleterious effect on cardiac output, • Possible exacerbation of myocardial ischemia, and • The risk of deterioration into VF.
  12. 12. II) Early Risk Stratification• High Risk Features include older age, low blood pressure, tachycardia, heart failure (HF), and an anterior MI.• Specific Scoring Systems, such as the TIMI Risk Score, permit a fairly precise determination of the risk of in-hospital mortality. (Morrow et al., 2001; Wu et al.,2002)
  13. 13. Early Risk Stratification• Patients at high risk are usually considered to require, Aggressive Management Strategy in addition to standard medical management.• Direct Transport or, less optimally, prompt Interhospital Transfer to a facility with revascularization capabilities is recommended for such patients. (Antman et al., 2004)
  14. 14. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  15. 15. The patient with an STEMI should be started ontherapy to: • Relieve ischemic pain, • Stabilize hemodynamic status, and • Reduce ischemia while being assessed as a candidate for Thrombolysis or Direct PCI. (Antman et al., 2004)
  16. 16. Other routine hospital measures include: • Anxiolytics, • Oxygen, • ECG, and BP monitoring, and • Intravenous access.All initial therapy can be carried out in the emergencydepartment based upon a predetermined, Institution-Specific, written protocol. (The 2004 ACC/AHA guidelines)
  17. 17. Reperfusion Therapy with either (PCI) orthrombolysis, if less than 12 hours has elapsed from theonset of symptoms. Primary PCI is preferred to thrombolysiswhen readily available. Antiplatelet Therapy includingaspirin, clopidogrel, and, in patients undergoing primaryPCI, a GP IIb/IIIa inhibitor. Sublingual Nitroglycerin followed by IV Nitroglycerinin patients with persistent chest pain after three sublingualnitroglycerin tablets, as well as in patients with hypertensionor HF.
  18. 18. Nitrates must be used with caution oravoided in settings in which hypotension is likely orcould result in serious hemodynamicdecompensation, such as RV Infarction or severeAortic Stenosis. Nitrates are contraindicated in patients whohave taken a phosphodiesterase inhibitor for erectiledysfunction within the previous 24 hours.
  19. 19. Intravenous Morphine Sulfate at an initial dose of 2to 4 mg, with increments of 2 to 8 mg repeated at 5 to 15minute intervals, to relieve chest pain and anxiety. Beta Blockers are administered universally to allpts without contraindications who experience an acuteSTEMI, irrespective of concomitant fibrinolytic therapy orperformance of primary PCI. Treatment should include Early Intravenous BetaBlockade. (Antman et al., 2004)
  20. 20. Electrolyte Replacement Although there are no clinical trials documentingthe benefits of Electrolyte Replacement in acuteMI, the ACC/AHA guidelines recommend maintainingthe serum Potassium concentration above 4.0 meq/Land a serum Magnesium concentration above 2.0meq/L (2.4 mg/dL or 1 mmol/L). (Antman et al., 2004)
  21. 21. Glucose Control Randomized trials have demonstrated that bothdiabetics and nondiabetics who have had an acute MI orare critically ill benefit from Tight Blood Glucose control. A class I recommendation to the use of an InsulinInfusion to normalize blood glucose in patients with anSTEMI and a complicated course, regardless of whetherthey have a diagnosis of diabetes mellitus (The 2004 ACC/AHA guidelines)
  22. 22. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  23. 23. Percutaneous Coronary Intervention PCIThe ACC/AHA task force gave a class I recommendationto the use of Primary PCI for:Any patient with an acute STEMI (defined as >1 mm STelevation in two contiguous leads after nitroglycerin to ruleout coronary vasospasm). • Who presents within 12 hours of symptom onset and • Who can undergo the procedure within 90 minutes of presentation. • By persons skilled in the procedure.
  24. 24. For patients presenting 12 to 24 hours aftersymptom onset, the performance of primary PCI isreasonable if the patient has: • Severe Heart Failure, • Hemodynamic or Electrical Instability, or • Persistent Ischemic Symptoms. (Antman et al., 2004)
  25. 25. All patients are pretreated at diagnosiswith aspirin, clopidogrel, and a GP IIb/IIIainhibitor. There appears to be No Role forPretreatment Thrombolysis before plannedprimary PCI (Facilitated PCI).
  26. 26. Recommended for:Any patient with an Acute Coronary Syndrome and:• ST elevation in at least two contiguous or adjacent leads,• New or presumably new LBBB, or• A true posterior MI.Who presents within 12 hours of symptom onset,• Has no contraindications for thrombolysis, and• Presents to a facility without the capability for expert, prompt intervention with primary PCI within 90 minutes of first medical contact. (Antman et al., 2004; Menon et al., 2004)
  27. 27. Indicated also for: Patients who present to a facility in which therelative delay necessary to perform primary PCI (theexpected Door-to-Balloon time minus the expecteddoor-to-needle time) is greater than one hour. The survival benefit is greatest when thrombolyticagents are administered within the first four hours afterthe onset of symptoms, particularly within the first 70minutes.
  28. 28. 1) The benefit of thrombolysis is greatest when therapy is given within the First Four Hours after the onset of symptoms, particularly within the first 70 minutes as the resistance of cross-linked fibrin is time-dependent (Boersma et al., 1996; Weaver et al., 1993)
  29. 29. 2) Although patency is restored in up to 87 percent of infarct-related arteries, normalization of blood flow (as assessed by the TIMI flow grade) occurs in only 50 to 60 percent. (The GUSTO Investigators et al., 1993; Chesebro et al., 1987)
  30. 30. 3) After apparently successful thrombolysis, Early Recurrence of Ischemia or ST segment shifts (Threatened Reocclusion) have been observed in 20 to 30 percent of patients, with frank Thrombotic Coronary Reocclusion in 5 to 15 percent, and reinfarction in 3 to 5 percent. (Gibson et al., 2003)
  31. 31. 4) Major Hemorrhagic Complications occur in 2 to 3 percent. The most serious is intracerebral hemorrhage, which occurs in: • As many as 1 percent overall, • 1.4 percent of the elderly, and • Over 4 percent in patients with multiple risk factors. (Brass et al., 2000)
  32. 32. 5) As many as 20 to 30 percent of patients presenting with an acute STEMI, particularly the elderly, are not candidates for thrombolytic therapy because of contraindications such as active internal bleeding, a recent stroke, or hypertension. (Cannon et al., 2002)
  33. 33. 6) Efficacy of Thrombolytic Therapy has not been demonstrated in patients in cardiogenic shock (unless coronary perfusion pressure is increased with an IABP) or those with prior coronary artery bypass surgery.
  34. 34. Recovery of LV function decreases with laterPCI, but late PCI may still be beneficial at a timewhen thrombolytic therapy is no longer effective. This is an important issue, since registry datasuggest that 9 to 31 percent of patients with an STEMIpresent more than 12 hours after the onset ofsymptoms. (Schomig et al., 2003)
  35. 35. Possible mechanisms for benefit:1) Residual antegrade or collateral blood flow, which was present in 73 percent of patients in the BRAVE-2 trial. The low rate of persistent flow may maintain myocardial viability and therefore infarct size until blood flow is restored by late PCI.2) Prevention of ventricular remodeling, also may be involved.3) A potential benefit of late primary PCI is a reduction in the risk of free wall rupture. (Gibbons et al., 2005)
  36. 36. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  37. 37. Intravenous Unfractionated HeparinIn the following patients: • Those with an STEMI undergoing PCI or surgical revascularization. • Those treated with thrombolytic therapy with alteplase, Release, or Tenecteplase. • Patients who receive No Reperfusion Therapy. (The ACC/AHA and ACCP guidelines) (Antman et al., 2004; Popma et al., 2004)
  38. 38. Low Molecular Weight Heparin• A class IIb recommendation: In patients with STEMI treated with thrombolytic therapy (usefulness or effectiveness is not well established).• It may be reasonable to use LMWH in patients who do not receive reperfusion therapy.• LMWH should be used only in patients under 75 yeas of age who are without significant renal dysfunction. (The ACC/AHA , 2004)
  39. 39. BivalirudinBivalirudin is an acceptable alternative to heparinplus GP IIb/IIIa inhibitor in patients undergoingprimary PCI (Initial bolus of 0.75 mg/kg IVfollowed by IV infusion of 1.75 mg/kg per hour;can be discontinued after PCI).
  40. 40. EnoxaparinEnoxaparin for patients not managed with PCIand <75 years give 30 mg IV bolus followedimmediately by 1 mg/kg subcutaneously every 12hours.In patients ≥75 years of age, do not use an initialIV bolus. Initiate dosing with 0.75 mg/kgsubcutaneous every 12 hours (maximum 75 mgfor the first two doses only).
  41. 41. Give antiplatelet therapy (in addition to aspirin)to all patients:1. Patients treated with fibrinolytic therapy: Give clopidogrel loading dose 300 mg if age less than 75 years; if age 75 years or older, give loading dose of 75 mg.2. Patients treated with no reperfusion therapy: Give ticagrelor loading dose 180 mg.
  42. 42. 3. Patients treated with primary percutaneous coronary intervention: Give ticagrelor loading dose of 180 mg or prasugrel loading dose of 60 mg (if no contraindications: prior stroke or TIA, or relative contraindications for prasugrel such as those age 75 years or older, weight less than 60 kg). For patients at high risk of bleeding, clopidogrel 300 to 600 mg (600 mg preferred) is preferred to ticagrelor or praugrel.
  43. 43. WarfarinIndications include: • Left Ventricular Thrombus Or Aneurysm. • Left Ventricular Ejection Fraction below 30 percent with or without heart failure. • A history of a thromboembolism. • Chronic Atrial Fibrillation, in which warfarin therapy is continued for an indefinite period of time.
  44. 44. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  45. 45. Prophylactic IV or ion Lidocaine to preventVT/VF in the acute MI patient is not recommended.Recommended prophylactic measures include: • Early administration of an intravenous Beta Blocker and • Correction of Hypokalemia and Hypomagnesemia.
  46. 46. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  47. 47. a) Oral Beta Blockers:An oral Cardioselective Beta Blocker, such as: • Metoprolol (25 to 50 mg BID with the short- acting preparation) or • Atenolol (50 to 100 mg daily),should be continued or begun if the patient has notreceived early intravenous therapy.
  48. 48. b) Nitrates:• Should be given for 24 to 48 hours in patients with: • Recurrent ischemia, • Hypertension, or • Heart failure.• Long-term Nitrate Therapy is useful for the treatment of Recurrent ischemia or Heart Failure.
  49. 49. c) ACE inhibitors:A class I recommendation is given to the administrationof oral ACE inhibitors within the first 24 hours of MI onsetin patients with the following characteristics. • ST elevation in two or more anterior precordial leads (anterior STEMI) • Clinical heart failure or pulmonary congestion • Left ventricular ejection fraction less than 40 percent (The ACC/AHA guidelines) (Antman et al., 2004)
  50. 50. Recommendation:An ACE inhibitor should be given to all patients withan STEMI without a contraindication. Treatmentshould be begun within the first 24 hours, sincethere is appreciable benefit in high-risk patients whocannot always be accurately identified in the first day. (Antman et al., 2004)
  51. 51. However, • Caution is necessary to avoid causing hypotension in the first few hours after the infarction. • Concern about concurrent aspirin therapy attenuating the effect of an ACE inhibitor appears largely unwarranted. (Latini et al., 2000)
  52. 52. d) Angiotensin II Receptor Blockers:The role for an Angiotensin II Receptor Blocker (ARB) inpatients with an STEMI is more limited.Class I Recommendation:In patients with an STEMI who are intolerant of ACEinhibitors and who have clinical or radiological signs ofheart failure or a left ventricular ejection fraction less than40 percent. (The 2004 ACC/AHA guidelines) (Antman et al., 2004)
  53. 53. e) Statin Therapy: Should be initiated prior to hospital discharge inall patients with an STEMI (Atorvastatin 80mg/day, which was used in the PROVE IT-TIMI 22 andMIRACL trials). (Antman et al., 2004) (Cannon et al., 2004) (Schwartz et al., 2001)
  54. 54. f) Calcium Channel Blockers: • Primarily serve as adjunctive therapy in patients with ongoing or recurrent symptoms of ischemia despite optimal therapy with beta blockers (with or without nitrates), • In patients who are unable to tolerate adequate doses of one or both of these agents, or • In patients with rapid AF when beta blockers are contraindicated.
  55. 55. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  56. 56. Coronary angiography and, if appropriate, PCI afterthrombolysis in patients with: • Recurrent MI, • Moderate or severe spontaneous or provocable myocardial ischemia during recovery, or • Cardiogenic Shock or Hemodynamic Instability. (A class I recommendation) The 2004 ACC/AHA guidelines)
  57. 57. I) Initial Assessment.II) Initial therapy.III) Reperfusion therapy.IV) Anticoagulation.V) Arrhythmia management.VI) Further medical therapy.VII) Angiography after thrombolysis.VIII) Managing recurrent chest pain.
  58. 58. Typically caused by either:• Recurrent Ischemia And Reinfarction Or• Infarction Pericarditis. Recurrent chest pain within the first 12 hours ofonset of MI is considered to be related to the originalinfarct and not evidence of reinfarction. Pericarditis is probably not responsible forsignificant chest discomfort in the first 24 hours.
  59. 59. Among patients with an STEMI who have undergoneapparently successful thrombolysis:• Early recurrence of ischemia (Threatened Reocclusion) has been observed in 20 to 30 percent of patients, (Armstrong et al., 1998; Langer et al., 1998)• Thrombotic Coronary Reocclusion in 5 to 15 percent, and (Topol et al., 1987; Ohman et al., 1990; The GUSTO Angiographic Investigators. 1993)• Reinfarction in 3 to 5 percent. (Gibson et al., 2003; Donges et al., 2001; Hudson et al., 2001; Barbash et al.,m 2001)
  60. 60. Therapeutic Strategy1. Escalation of Therapy: with beta blockers and nitrates to decrease myocardial oxygen demand and reduce ischemia.2. Intravenous Anticoagulation: should be initiated if it is not already being administered.3. Insertion Of An Intraaortic Balloon Pump should also be considered for patients with: • Hemodynamic instability, • Poor LV function, or • A large area of myocardium at risk. (Antman et al., 2004)
  61. 61. Management Strategy:4. PCI is the treatment of choice for patients with recurrent ischemia or emergent CABG for reinfarction or threatened reinfarction in the following settings, provided that coronary anatomy is suitable: • When there is objective evidence of recurrent MI. • For moderate or severe spontaneous or provocable ischemia. • For cardiogenic shock or hemodynamic instability. (The ACC/AHA guidelines a class I recommendation) (Antman et al., 2004)
  62. 62. Management Strategy:5. Patients with recurrent ST elevation can also be treated or retreated with Thrombolytic Therapy. However, an invasive strategy of angiography and revascularization is usually preferred. Patients should not be Retreated with Streptokinase. (Antman et al., 2004; Barbash et al., 2001)
  63. 63. 1. Heart Failure and Cardiogenic Shock:  Class III patients should be considered for hemodynamic monitoring if they do not respond promptly to medical therapy.  Killip class IV patients generally require invasive monitoring with pulmonary artery catheterization and arterial blood pressure monitoring.
  64. 64. Heart Failure and Cardiogenic Shock:Invasive hemodynamic monitoring may also bewarranted for patients with suspected mechanicalcomplications of MI resulting in shock, such as:  Papillary muscle rupture or Dysfunction,  Ventricular septal defect, or  Cardiac tamponade.
  65. 65. Killip-Kimball Hemodynamic SubsetsClass Description I No dyspnea; physical examination results are normal II No dyspnea; bibasilar crackles or S3 on examination Dyspnea present; bibasilar crackles or S3 on III examination; no hypotension IV Cardiogenic shock
  66. 66. Pharmacologic Treatment:Should be tailored to the patients clinical and hemodynamicstate.Patients with:  Systolic arterial pressure >100 mmHg,  Pulmonary artery occlusion pressure >15 mm Hg, and  Cardiac index <2.5 L/min/mz.Should be treated initially with a vasodilator, eitherintravenous nitroglycerin or intravenous nitroprusside.
  67. 67. Inotropic support: If arterial pressure decreases or the increase incardiac output is inadequate, inotropic support withdobutamine should be initiated at 1 to 2 pg/kg/min andtitrated to 5_15 pg/kg/min. Milrinone is an alternativeinotropic agent. Loop diuretics, such as furosemide (20-40 mgintravenously or orally every 2-4 hours), should be used toreduce pulmonary congestion. Diuretics should be usedwith caution in hypotensive patients.
  68. 68.  Systolic arterial pressure <90 mm Hg, Pulmonary arterial occlusion pressure >15 mm Hg, and Cardiac index <2.5 L/min/m2. These patients should be treated as soon as possible with Intra-aortic Balloon Counterpulsation (IABC).
  69. 69. Severely hypotensive patients (systolic arterialpressure <70 mmHg) should be treated withnorepinephrine to rapidly raise the systolic arterialpressure. If the systolic arterial pressure is 70 to 90 mmHgwith signs of shock, dopamine may be considered initially. Once the systolic blood pressure has stabilized to atleast 90 mm Hg, dobutamine can be added to furtherincrease cardiac output and reduce the dosage ofvasopressor.
  70. 70. Patients with STEMI who develop shock within 36hours of MI:  Benefit from Early Invasive Reperfusion performed within 18 hours of onset of shock.  In patients with 1- or 2-vessel disease, PCI is preferred.  Patients who remain symptomatic and have 3-vessel disease or significant left main coronary artery disease should undergo urgent coronary bypass surgery.
  71. 71.  Volume Expansion until the blood pressure is stabilized, pulmonary arterial occlusion pressure is >20 mmHg, or right atrial pressure is >20 mmHg. Associated Bradycardia or high-degree heart block may require chemical or electrical intervention.
  72. 72.  Agents such as nitrates and diuretics that reduce preload should be avoided. If volume expansion is inadequate to stabilize a patient, dobutamine can be administered. lntra-aortic balloon counterpulsation should - be considered for refractory hypotension.
  73. 73.  Occurs in < 20% of patients treated with thrombolytic therapy. Patients treated with primary PCI have a lower incidence of recurrent ischemia. Reinfarction may present special diagnostic difficulties (cardiac troponin levels can be elevated for 5 to 14 days). Pericarditis should also be considered as a potential cause of recurrent chest pain after an MI.
  74. 74.  Medical treatment is similar to management of unstable angina. But also includes cardiac catheterization and reperfusion, Recurrent infarction with ST elevation on ECG can be treated with repeat thrornbolysis. Streptokinase- based drugs should not be used a second time because of the risk of allergic reactions. Acute reperfusion with PCI or CABG maybe required for stabilization.
  75. 75. Hemodynamically significant bradycardia or A-V Block: Can be initially treated with intravenousatropine in a dose of 0.5 mg every 3-5 minutes toa total dose of 3 mg while preparing fortranscutaneous pacing. Atropine rarely corrects complete heartblock or type II second-degree A-V block.
  76. 76. Temporary Transvenous Pacing is indicated for: Complete heart block, Bilateral Bundle Branch Block, New or indeterminate-age Bifascicular Block with first- degree A-V block, Type II second-degree AN block, and Symptomatic sinus bradycardia that is unresponsive to atropine.
  77. 77.  Immediate Cardioversion is indicated in unstable patients. Depending upon the specific arrhythmia, intravenous adenosine, b-blockers, or diltiazem may be effective. Ventricular tachycardia and ventricular fibrillation should be treated according to current ACLS guidelines. After defibrillation, if indicated, amiodarone is the drug of choice in patients with an MI.
  78. 78.  Can occur prior to surgery, intraoperatively, and during the postoperative period. Postoperative MI is the most common, with the peak incidence on the third postoperative day. Perioperative MI is often associated with atypical presentations and is frequently painless. New-onset, or an increase in, Ventricular Arrhythmias is often the presenting finding, as is postoperative Pulmonary Edema.
  79. 79.  The diagnosis can be confirmed with serial ECG and cardiac marker determinations. Treatment is similar to standard treatment. Thrombolytic therapy may be contraindicated depending on the type of surgery. Primary PCI should be considered. The mortality for perioperative MI is very high, up to 60% in some studies.
  80. 80. 1. The preliminary diagnosis of unstable angina/non-ST-elevation MI is based on the clinical symptoms, assessment of risk factors for coronary artery disease, and ECG interpretation.2. A 12-lead ECG should be obtained and interpreted within 10 minutes in patients with possible myocardial ischemia.3. Non-enteric-coated aspirin at a dose of 162 to 325 mg should be initially administered (by chewing) as soon as possible to all patients with suspected or diagnosed ACS.
  81. 81. 4. High-risk patients (continuing ischemia, elevated troponin levels) with UA/NSTEMI may be candidates for additional therapy with (GP) IIb/lIIa inhibitors and an early invasive strategy.5. The combination of aspirin and heparin is more beneficial in ACS than aspirin alone.6. b-Blockers should be administered to all patients with ACS unless there are strong contraindications.
  82. 82. 7. A plan for early reperfusion of patients with STEMI should be developed by healthcare providers based on resources available in their facility and community.8. A goal of 90 minutes or less from hospital presentation to balloon inflation is optimum for primary PCI for STEMI.9. Thrombolytic therapy for reperfusion in SIEMI should ideally be initiated within 30 minutes of the patients arrival to the hospital.
  83. 83. 10. Patients who undergo PCI with angioplasty with or without stent placement should be treated with a GP IIb/IIIa inhibitor and an antiplatelet agent such as clopidogrel.11. Use of angiotensin-converting enzyme inhibitdrs decreases mortality in all patients with STEMI.12. Evidence suggests that patients with STEMI who develop shock within 36 hours of MI benefit from early invasive reperfusion performed within 18 hours of onset of shock.
  84. 84. Myocardial infarction (MI) with LV failureremains the most common cause of CS. Ingeneral, CS complicates 8.6% of ST-segmentelevation MIs (STEMI)2 and 2.5% of non–STsegment elevation MIs.3 (Hasdai et al., 2000)
  85. 85. It is increasingly clear that CS represents a wideclinical spectrum, including preshock (patients atsignificant risk of developing CS), mild CS(responsive to low-dose inotropes/vasopressors),profound CS (responsive to high-dose inotropes/vasopressors and IABP, and severe refractory CS(SRCS; unresponsive to high-dose inotropes/vasopressors and IABP).
  86. 86. The first published clinical trial of IABPs inpatients with CS demonstrated augmentationof cardiac output by 0.5 L/min7. (Scheidt et al., 1973)
  87. 87. Subsequent data from the Should WeEmergently Revascularize Occluded Coronariesfor Cardiogenic Shock (SHOCK) Trial Registrydemonstrated lower in-hospital mortality inpatients with MI who received IABP incombination with thrombolytic therapy or earlyrevascularization with percutaneous transluminalcoronary angioplasty/coronary artery bypassgraft surgery8. (Sanborn et al., 2000)
  88. 88. Similarly, in the Global Utilization ofStreptokinase and TPA for Occluded CoronaryArteries (GUSTO-I) trial, early institution of IABPand thrombolytic therapy in patients with acuteMI (AMI) complicated by CS was associated withan increased risk of bleeding and adverseevents but also a trend toward lower 3-day and1-year all-cause mortality9. (Anderson et al., 1997)
  89. 89. Common Causes of Cardiogenic ShockMI without mechanical complicationsMI with mechanical complications (ventricularseptal rupture or papillary muscle/chordal rupture).Acute decompensation of chronic heart failure
  90. 90. Common Causes of Cardiogenic ShockAcute myocarditiesPostcardiotomyTakotsubo/stress-induced cardiomyopathyPeripartum cardiomyopahty
  91. 91. Common Causes of Cardiogenic ShockRefractory arrhythmiasCardiac tamponadeMassive pulmonary embolism
  92. 92. Common Causes of Cardiogenic ShockAcute rejection after orthotopic hearttransplantationHypertrophic cardiomyopathy with severe outflowobstructionAortic dissection complicated by acute severeaortic insufficiency and/or MI
  93. 93. A recent meta-analysis suggested thatalthough IABPs may have a beneficial effecton hemodynamic parameters in infarct-related CS, the existing data to not support amortality benefit12. (Unverzagt et al., 2011)
  94. 94. Finally, another recent meta-analysisevaluating the use of IABPs in patients withSTEMI complicated by CS suggested noimprovement in 30-day survival or LV ejectionfraction and an increased risk of stroke andbleeding complications13. (Sjauw et al., 2009)
  95. 95. Given the minimal circulatory supportafforded by IABPs, next generation ofexternal VADs was designed to be surgicallyimplanted and powerful enough to provide fullcirculatory support.
  96. 96. Despite advances in surgically implantedexternal VAD technology and improvement inthe morbidity and mortality attributable tothese devices, important clinical problemremain.
  97. 97. Including the need for generalanesthesia, systemic inflammation associatedwith an open surgical procedure, and theoften prolonged delay associated withoperating room activation.
  98. 98. Widely regarded as the first PVAD, theHemopump Cardiac Assist System (Johnsonand Johnson Interventional Systems. RanchoCordova, CA) was a catheter-mounted, axialflow device positioned across the aortic valveand capable of providing up to 3.5 L/min ofshort-term (hours to days) cardiac support forpatients with CS25. (Wampler et al., 1994)
  99. 99. The TendemHeart PVAD(CardiaAssist, Inc, Pittsburgh, PA) is a leftatrial-femoral bypass centrifugal pumpcapable of providing up to 3.5 to 4.5 L/min ofcardiac output when inserted percutaneously.
  100. 100. Inflow/outflow cannulaconfigurations for the TandemHeart and Impella Recover 2.5 percutaneous ventricular assist devices (PVADs)
  101. 101. Although ECMO technology was developedin the 1960s, there has been a recentresurgence of this technology owing to bettercannulation techniques, smallercannulas, improved oxygenatormachines, and device miniaturization.
  102. 102. Together, these improvements have resultedin lightweight, portable, reliable, and rapidlyimplantable percutaneous ECMO systems in2 possible configurations: veno-venous forpulmonary support and veno-arterial forcardiac and pulmonary support.
  103. 103. The major advantage of these systems overother modern PVADs is the lack of need fortransseptal puncture or transfer to a cardiaccatheterization laboratory.

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