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Inadequate tissue perfusion resulting from cardiac dysfunction

SCCM Online Critical Care Course: Cardiogenic Shock, Acute Coronary Syndrome and Congestive Heart Failure. Cardiogenic Shock. Inadequate tissue perfusion resulting from cardiac dysfunction

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Inadequate tissue perfusion resulting from cardiac dysfunction

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  1. SCCM Online Critical Care Course: Cardiogenic Shock, Acute Coronary Syndrome and Congestive Heart Failure

  2. Cardiogenic Shock • Inadequate tissue perfusion resulting from cardiac dysfunction • Clinical definition - decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume • Hemodynamic definition - sustained systolic BP < 90 mm Hg, cardiac index < 2.2 L/min/m2, PCWP > 15 mm Hg Parrillo, J. 2005

  3. Causes of Cardiogenic Shock • Acute MI • Pump failure • Mechanical complications • Right ventricular infarction • Other conditions • End-stage cardiomyopathy • Myocarditis (fulminant myocarditis) • Myocardial contusion • Prolonged cardiopulmonary bypass • Septic shock with myocardial depression • Valvular disease

  4. Cardiogenic Shock Evolution Of The Disease Frequently, shock develops after presentation for myocardial infarction. - SHOCK Registry • At presentation 25% in shock • Within 24 hours 75% (median delay = 7 hours) - GUSTO Trial • At presentation 11% in shock • After admission 89% SHOCK Registry, Circulation. 1995;91:873-81. GUSTO J Amer Coll Cardiol. 1995;26:668-74.

  5. Schematic Diagram of StunnedMyocardium Clamp Wall motion abnormality Wall motion abnormality during occlusion Coronary occlusion Coronary reperfusion Persistent wall motion abnormality (despite reperfusion and viable myocytes) Return of function Gradual return of function (hours to days) From Kloner RA. Am J Med. 1986;86:14.

  6. Hibernating Myocardium Wall motion abnormality Atherosclerotic narrowing Wall motion abnormality due to chronic ischemia without infarction From Kloner RA. Am J Med. 1986;86:14.

  7. Hibernating Myocardium 8 Months Postoperative Pre-operative Single vessel disease - Occluded L.A.D. Patient Coronary Bypass Graft to L.A.D. CONTROL LVEDV = 128 EF = 0.37 POST NTG LVEDV = 101 EF = 0.51 LVEDV = 104 EF = 0.76 End-Diastole End-Systole From Rahimtoola SH, et al. Circ. 1992;65:225.

  8. Ischemic Myocardium Cell death Reperfusion Significant residual stenosis Segments withmyocardialstunning Segments withboth stunningand hibernation Segments withhibernatingmyocardium Inotropicsupport Relief of ischemia No returnof function Return ofmyocardial function

  9. Initial Approach: Management • Assure oxygenation • Intubation and ventilation if needed • Venous access • Pain relief • Continuous EKG monitoring • Hemodynamic support • Fluid challenge if no pulmonary edema • Vasopressors for hypotension - Dopamine - Norepinephrine

  10. Intra-aortic Balloon Counterpulsation • Reduces afterload and augments diastolic perfusion pressure • Beneficial effects occur without increase in oxygen demand • No improvement in blood flow distal to critical coronary stenosis • No improvement in survival when used alone • May be essential support mechanism to allow for definitive therapy

  11. Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock Overall 30-Day Survival in the Study 1.0 0.8 Revascularization (n =152) Survival= 53% 0.6 Proportion Alive 0.4 Medicaltherapy (n =150) Survival =44% 0.2 p = 0.11 0.0 0 5 10 15 20 25 30 Days after Randomization Hochman JS, et al. N Engl J Med. 1999;341:625-34.

  12. SHOCK Trial Mortality 100 P = 0.11 P = 0.027 P < 0.03 80 66.4 63.1 % 56 60 54.3 50.3 46.7 40 Revasc MedRx 20 0 30 days 1 year 6 months

  13. ACC/AHA Class I Indication • Patients with ST segment elevation MI who have cardiogenic shock and are less than 75 years of age should be brought immediately or secondarily transferred to facilities capable of cardiac catheterization and rapid revascularization (PCI or CABG) if it can be performed within 18 hours of onset of shock. (Level of Evidence: A)

  14. National Registry of MI Early Revascularization is Underutilized in Cardiogenic Shock • Despite ACC/AHA recommendation to treat patients < 75 years of age aggressively with early mechanical revascularization, in 2001, two years after the guidelines were published, only 41% of patients with cardiogenic shock complicating AMI were treated with primary PTCA and only 3.1% underwent early CABG. • These data demonstrate significant underutilization of guideline recommended therapy. Babaev A, et al. Circ. 2002;106(19):1811 (abstract).

  15. Pathophysiology of Cardiogenic Shock Observations from the SHOCK Trial and Registry that Challenge the Classic Paradigm • Average LVEF is only moderately severely depressed (30%), with a wide range of EFs and LV sizes noted. • Systemic vascular resistance (SVR) on vasopressors is not elevated on average (~ 1350), with a very wide range of SVRs measured. • A clinically evident systemic inflammatory response syndrome is often present in patients with CS. • Most survivors (85%) have NYHA functional Class I-II CHF status. Hochman JS. Circ .2003;107:2998-3002.

  16. Pathophysiology of Cardiogenic Shock • Cardiogenic shock IS NOT simply the result of severe depression of LV function due to extensive myocardial ischemia/injury. • Depressed Myocardial Contractility combined with Inadequate Systemic Vasoconstriction resulting from a systemic inflammatory response to extensive myocardial ischemia/injury results in cardiogenic shock .

  17. The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation. Thus, excess nitric oxide and peroxy nitrites may be a major contributor to cardiogenic shock complicating MI.

  18. LINCS: Conclusions • Nitric oxide synthase inhibition can raise blood pressure in patients with persistent cardiogenic shock after percutaneous intervention. • The mechanism of this effect is unknown, but may involve both an effect on coronary and other organ perfusion pressure, and potentially an improvement in cardiac function. • Outcome data are not yet available. Cotter. Eur Heart J. 2003;24:1287-1295.

  19. Acute Coronary Syndromes: Definitions Acute coronary syndrome: Constellation of clinical symptoms compatible with acute myocardial ischemia • ST-segment elevation MI (STEMI) • Non-ST-segment elevation MI (NSTEMI) • Unstable angina Unstable angina: • Angina at rest (usually > 20 minutes) • New-onset of class III or IV angina • Increasing angina (from class I or II to III or IV) Braunwald. Circulation 2002; 106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  20. Pathogenesis of Acute Coronary Syndromes Plaque rupture Platelet adhesion Platelet activation Partially occlusive arterial thrombosis & unstable angina Microembolization & non-ST-segment elevation MI Totally occlusive arterial thrombosis & ST-segment elevation MI White HD. Am J Cardiol 1997;80 (4A):2B-10B.

  21. Structure of Thrombus Following Plaque Disruption UA/NSTEMI:Partially-occlusive thrombus (primarily platelets) STEMI:Occlusive thrombus (platelets, red blood cells, and fibrin) Intra-plaque thrombus (platelet-dominated) Intra-plaque thrombus (platelet-dominated) Plaque core Plaque core UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction SUDDEN DEATH White HD. Am J Cardiol 1997;80 (4A):2B-10B.

  22. Diagnostic Algorithm for Acute Coronary Syndrome Management + Troponinor + CK-MB &/or ST-segment elevation MI Non-ST Elevation ACS* Non-ST Elevation MI Therapeutic goal: rapidly break apart fibrin mesh to quickly restore blood flow Therapeutic goal: prevent progression to complete occlusion of coronary artery and resultant MI or death Consider fibrinolytic therapy, if indicated, or primary percutaneous coronary intervention (PCI) Consider GP IIb-IIIa inhibitor + aspirin + heparin before early diagnostic catheterization Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.

  23. 0.25 0.20 0.15 0.10 0.05 0.00 Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin in Men with Unstable CAD Placebo Probabilityof Death or MI Aspirin 75 mg Risk ratio 0.5295% CL 0.37 - 0.72 0 3 6 9 12 Months Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93.

  24. Low Molecular Weight Heparin (LMWH) vs. Unfractionated Haparin (UFH) in Non-ST elevation ACS: Effect on Death, MI, Recurrent Ischemia Day: Trial: FRIC (Dalteparin; n = 1,482) FRAXIS (nadroparin; n = 2,357) ESSENCE (enoxaparin; n = 3,171) TIMI 11B (enoxaparin; n = 3,910)  6  14 (p= 0.032) 14  (p= 0.029) 14  .751.0 1.5 LMWH Better UFH Better Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  25. Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment Elevation % 14 11.4% Placebo + ASA 12 9.3% 10 8 Clopidogrel + ASA Death, MI, or Stroke 6 4 20% RRR P < 0.001 N = 12,562 2 0 0 3 6 9 12 Months of Follow-Up N Engl J Med. 2001;345:494-502.

  26. Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials 20 Placebo 17.9 GP IIb/IIIa 15.7 14.2 15 12.9 12.8 11.8 11.7 10.3 10 Primary Endpoint % 5.6 5 3.8 P = 0.04 P = 0.01 P = 0.004 P = 0.48 P = 0.33 0 PURSUIT30 days PRISM48 hrs PRISM PLUS7 days PARAGON A30 days PARAGON B30 days

  27. I IIa IIb III Hospital CareAnti-Thrombotic Therapy Immediate aspirin Clopidogrel, if aspirin contraindicated Aspirin + clopidogrel for up to one month, if medical therapy or PCI is planned Heparin (IV unfractionated, LMW) with antiplatelet agents listed above Enoxaparin preferred over UFH unless CABG is planned within 24 hours Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  28. I IIa IIb III Hospital CareClopidogrel Therapy Aspirin + clopidogrel, for up to 1 month * Aspirin + clopidogrel, for up to 9 months * Withhold clopidogrel for 5 - 7 days for CABG Guidelines do not specify initial approach to using clopidogrel when coronary anatomy is unknown * For patients managed with an early conservative strategy, and those who are planned to undergo early PCI Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  29. I IIa IIb III Hospital CarePlatelet GP IIb/IIIa Inhibitors (1) Any GP IIb/IIIa inhibitor + ASA/Heparin for all patients, if cath/PCI planned Eptifibatide or tirofiban + ASA/Heparin for high-risk * patients in whom early cath/PCI is not planned Any GP IIb/IIIa inhibitor for patients already on ASA + Heparin + clopidogrel, if cath/PCI is planned * High-risk: Age >75; prolonged, ongoing CP; hemodynamic instability; rest CP w/ ST ; VT; positive cardiac markers Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  30. I IIa IIb III Hospital CarePlatelet GP IIb/IIIa Inhibitors (2) Eptifibatide or tirofiban + ASA/Heparin for patients without continuing ischemia in whom PCI is not planned Abciximab for patients in whom PCI is not planned Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  31. I IIa IIb III Hospital CareAnti-ischemic Therapy (1) -blocker (IVoral) if not contraindicated Non-dihydropyridine Ca2+ antagonist if -blocker contraindicated and no LV dysfunction, for recurrent ischemia ACE inhibitor if  BP persists with NTG+ -blocker, for pts with CHF or diabetes Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  32. I IIa IIb III Hospital CareAnti-ischemic Therapy (2) ACE inhibitor for all ACS pts Extended-release Ca2+ blocker instead of -blocker Immediate-release Ca2+ blocker with -blocker Long-acting Ca2+ blocker for recurrent ischemia, if no contraindications and NTG + -blocker used fully Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  33. 10% 8% 6% 4% 2% ST-segment Depression PredictsHigher Risk of Mortality in ACS % Cumulative Mortality at 6 Months ST-segment depression8.9% ST-segment elevation6.8% T-wave inversion3.4% 30 60 90 120 150 180 Days from randomization Savonitto S. J Am Med Assoc. 1999; 281: 707-711.

  34. TIMI Risk Score for UA/NSTEMI7 Independent Predictors of Higher Risk • Age > 65 years 2. > 3 CAD risk factors (elevated cholesterol, + family Hx, hypertension, diabetes, cigarette smoking) 3. Prior CAD (coronary stenosis > 50%) 4. ASA in last 7 days 5. > 2 anginal events < 24 hours 6. ST deviation 7. Elevated cardiac markers (CK - MB or troponin) Antman, et al. JAMA. 2000;284:835-842.

  35. TIMI UA Risk Score:Primary Endpoint at 6 months OR = 0.55 CI (0.33, 0.91) CONS INV OR = 0.75 CI (0.57, 1.00) Death/MI/ACS Rehosp (%) TIMI Risk Score % of Pts: 25% 60% 15%

  36. Troponin and ST-Segment Shift PredictBenefit of Invasive Treatment Strategy Cannon. J Invas Cardiol. 2003;15:22B.

  37. ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI Class I Anearly invasivestrategy in patients with ahigh-riskindicator: Recurrent angina/ischemia despite intensive anti-ischemic rx Elevated troponin-T or troponin-I New or presumably new ST-segment depression Recurrent angina/ischemia with CHF sx, S3, pulmonary edema, worsening rales, or new or worsening MR 5. High-risk findings on noninvasive stress testing 6. Depressed LV systolic function (EF <40%) 7. Hemodynamic instability 8. Sustained ventricular tachycardia 9. PCI within 6 months 10. Prior CABG Either early invasive or early conservative strategy ifnot high risk Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  38. 2002 ACC/AHA Guidelines for theManagement of High-risk NSTE ACS At presentationST-segment depression &/or elevated cardiac troponin Need to immediately arrest thrombus progression Need to eliminate occlusive ruptured plaque • Start immediate • Aspirin • Heparin or low-molecular-weight heparin • GP IIb-IIIa inhibitor Send for catheterization & revascularization within 24-48 hours • Cautionary information • No clopidogrel within 5-7 days prior to CABG surgery • No enoxaparin within 24 hours prior to CABG surgery • No abciximab, if PCI is not planned Adapted from Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.

  39. Ongoing Evaluation in an EarlyConservative Strategy Early medical management Patient stabilizes Recurrent Symptoms/ischemia Heart failure Serious arrhythmia Evaluate LV function EF < .40 EF  .40 Stress Test Low risk Not low risk Follow on Medical Rx Immediate angiography Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.

  40. Early conservative strategy Early invasive strategy 12-24 hour angiography Patient stabilizes EF > .40 Stress Test ACC/AHA Guidelines for Unstable Angina and Non-ST-Segment Elevation MI Acute Ischemia Pathway ST , positive cardiac markers, deep T-wave inversion, transient ST , or recurrent ischemia Aspirin, Beta Blockers, Nitrates, Antithrombin regimen, GP IIb-IIIa inhibitor, Monitoring (rhythm and ischemia) Immediate angiography Recurrent symptoms/ischemia Heart failure Serious arrhythmia Evaluate LV Function EF < .40 Not low risk Low risk Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf Follow on Medical Rx

  41. ACC/AHA Guidelines for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI Class I indications for revascularizationwith PCI or CABG 1. CABG for  50% stenosis of the left main coronary artery 2. CABG for 3 vessel CAD 3. CABG for 2 vessel CAD including proximal LAD stenosis & EF < 50% 4. PCI or CABG for 1 or 2 vessel CAD, no proximal LAD, large area of viability, high-risk noninvasive test 5. PCI for patients with multivessel CAD, normal EF, no diabetes 6. IV platelet GP IIb/IIIa inhibitor in ACS patients undergoing PCI Braunwald. Circulation 2002; 106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  42. ACC/AHA Guidelines for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI Class IIa indications for revascularizationwith PCI or CABG 1. Repeat CABG for patients with multiple saphenous vein graft stenoses, especially if LAD graft 2. PCI for focal saphenous vein graft lesions or multiple lesions if poor surgical candidate 3. PCI or CABG for patients with 1 or 2 vessel CAD, not proximal LAD, but moderate area of viability and ischemia 4. PCI or CABG for patients with 1 vessel CAD with proximal LAD 5. CABG with Internal Mammary artery for patients with multivessel CAD and diabetes Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  43. Recommendations for Revascularization Cardiac Catheterization Discharge from Protocol Coronary Artery Disease NO Left Main Disease YES CABG NO 3 Vessel Disease or 2 Vessel Disease with proximal LAD involvement 1 or 2 Vessel Disease Left Ventricular Dysfunction or Treated Diabetes CABG PCI or CABG, if eligible YES NO PCI or CABG Smith et al. ACC/AHA PCI Guidelines. J Am Coll Cardiol 2001:2239-lxvi.

  44. UA/NSTEMI ASA, Heparin/Enox.,   block., Nitrates, Clopidogrel RISK STRATIFY Low Risk High Risk * ACC/AHA REVISED GUIDELINES * Recurrent ischemia; Trop; ST; LV failure/dysf.; hemodynamic instability; VT; prior CABG  Enoxeparin. Preferred to UFH (IIa) If coronary arteriography >24 hours Braunwald E, et al. Circ. 2002;106:1893.

  45. High Risk Cor. Arteriography LMCD, 3VD+LV Dys., or Diab. Mell. 1 or 2VD, Suitable for PCI Normal CABG Consider Alternative Diagnosis Clopidogrel, IIb/IIIa inhib. PCI Discharge on ASA, Clopidogrel, Statin, ACEI ACC/AHA REVISED GUIDELINES Braunwald E, et al. Circ. 2002;106:1893.

  46. I IIa IIb III Discharge/Post-discharge Medications ASA, if not contraindicated Clopidogrel, when ASA contraindicated Aspirin + Clopidogrel, for up to 9 months -blocker, if not contraindicated Lipid  agents (statins) + diet ACE Inhibitor: CHF, EF < 40%, DM, or HTN Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf

  47. All-Cause Death or Major Cardiovascular Events in All Randomized Subjects 30 Pravastatin 40 mg (26.3%) 25 20 Atorvastatin 80 mg (22.4%) % with Event 15 10 16% RR (P = 0.005) 5 0 3 6 9 12 15 18 21 24 27 30 0 Months of follow up Cannon CP, et al. N Engl J Med. 2004;350:1495-1504.

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