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Cardiogenic Shock, Acute Coronary Syndrome, Congestive  Heart Failure, and Arrhythmias Dalhousie Critical Care Lecture Series
[object Object],[object Object],[object Object],Parrillo, J.  2005 Cardiogenic Shock
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Causes of 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 . Cardiogenic Shock
Wall motion  abnormality during occlusion Wall motion abnormality From Kloner RA. Am J Med. 1986;86:14. Gradual return of function (hours to days) Persistent wall motion abnormality (despite reperfusion and viable myocytes) Coronary occlusion Coronary reperfusion Return of function Clamp Schematic Diagram of Stunned Myocardium
Cell death Significant residual stenosis Reperfusion Segments with myocardial stunning Segments with both stunning and hibernation Segments with hibernating myocardium Relief of  ischemia Inotropic support No return of function Return of myocardial function Ischemic Myocardium
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Initial Approach: Management
Dopamine ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Dobutamine ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Epinepherine ,[object Object],[object Object],[object Object],[object Object]
Milrinone ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Norepinepherine ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Use of Inotropes ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Use of Vasopressors ,[object Object],[object Object],[object Object]
Intra-aortic Balloon Counterpulsation
[object Object],[object Object],[object Object],[object Object],[object Object],Intra-aortic Balloon Counterpulsation
Overall 30-Day Survival in the Study Hochman JS, et al. N Engl J Med. 1999;341:625-34. Proportion Alive 0 Days after Randomization 0.6 0.2 0.0 0.8 Revascularization (n =152) Medical   therapy (n =150) 1.0 0.4 5 10 15 20 25 30 Survival   = 53% Survival =   44% p = 0.11 Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock
46.7 50.3 54.3 56 63.1 66.4 0 20 40 60 80 100 % P = 0.11 P = 0.027 P < 0.03 30 days 6 months 1 year Revasc Med   Rx SHOCK Trial Mortality
[object Object],ACC/AHA Class I Indication
[object Object],[object Object],[object Object],[object Object],Hochman JS. Circ .2003;107:2998-3002.  Pathophysiology of Cardiogenic Shock Observations from the SHOCK Trial and Registry that Challenge the Classic Paradigm
[object Object],[object Object],Pathophysiology of Cardiogenic Shock
Thus, excess nitric oxide and peroxy nitrites may be a major contributor to cardiogenic shock complicating MI. The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Acute Coronary Syndromes: Definitions
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. Pathogenesis of Acute Coronary Syndromes
UA/NSTEMI: Partially-occlusive thrombus (primarily platelets) Intra-plaque  thrombus  (platelet-dominated) Plaque core STEMI: Occlusive thrombus (platelets,  red blood cells, and fibrin) Intra-plaque  thrombus  (platelet-dominated) Plaque core SUDDEN DEATH UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction Structure of Thrombus Following Plaque Disruption White HD. Am J Cardiol 1997;80 (4A):2B-10B.
Therapeutic goal: rapidly break apart fibrin mesh to quickly restore blood flow ST-segment elevation MI Non-ST Elevation ACS* Non-ST Elevation MI + T roponin or + CK-MB Consider fibrinolytic therapy, if indicated, or primary percutaneous coronary intervention (PCI) Therapeutic goal: prevent progression to complete occlusion of coronary artery and resultant MI or death Consider GP IIb-IIIa inhibitor + aspirin + heparin before early diagnostic catheterization &/or Braunwald E, et al. 2002.  http://www.acc.org/clinical/guidelines/unstable/unstable.pdf . Diagnostic Algorithm for Acute Coronary Syndrome Management
0 3 6 9 12 Probability of Death or MI Placebo Aspirin 75 mg Risk ratio 0.52 95% CL 0.37 - 0.72 Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin in Men with Unstable CAD Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93. Months 0.00 0.05 0.10 0.15 0.20 0.25
Trial: FRIC (Dalteparin; n = 1,482) FRAXIS (nadroparin; n = 2,357) ESSENCE (enoxaparin; n = 3,171) TIMI 11B (enoxaparin; n = 3,910) .75 1.0 1.5     (p= 0.032) (p= 0.029) LMWH Better UFH Better 6 14 14 14 Day: Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf Low Molecular Weight Heparin (LMWH) vs. Unfractionated Haparin (UFH) in Non-ST elevation ACS: Effect on Death, MI, Recurrent Ischemia
0 2 4 6 8 10 12 14 Death, MI, or Stroke Clopidogrel  + ASA 3 6 9 Placebo  + ASA Months of Follow-Up 11.4% 9.3% 20% RRR P  < 0.001 N = 12,562 0 12 % N Engl J Med. 2001;345:494-502. Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment Elevation
15.7 5.6 17.9 11.7 12.8 14.2 3.8 12.9 10.3 11.8 0 5 10 15 20 Primary Endpoint % Placebo GP IIb/IIIa PURSUIT 30 days PRISM 48 hrs PRISM PLUS 7 days P = 0.04 P = 0.01 P = 0.004 PARAGON A 30 days P = 0.48 PARAGON B 30 days P = 0.33 Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials
30 60 90 120 150 180 T-wave inversion 3.4% ST-segment elevation 6.8% ST-segment depression 8.9% Days from randomization % Cumulative Mortality at 6 Months Savonitto S. J Am Med Assoc. 1999; 281: 707-711. ST-segment Depression Predicts Higher Risk of Mortality in ACS 10% 8% 6% 4% 2%
 
Cannon. J Invas Cardiol. 2003;15:22B. Troponin and ST-Segment Shift Predict Benefit of Invasive Treatment Strategy
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI
[object Object],[object Object],[object Object],[object Object],Adapted from Braunwald E, et al. 2002.  http://www.acc.org/clinical/guidelines/unstable/unstable.pdf . At presentation ST-segment depression &/or elevated cardiac troponin Need to immediately arrest thrombus progression Need to eliminate occlusive  ruptured plaque Send for catheterization & revascularization within 24-48 hours ,[object Object],[object Object],[object Object],[object Object],2002 ACC/AHA Guidelines for the Management of High-risk NSTE ACS
Recurrent  Symptoms/ischemia Heart failure Serious arrhythmia Patient  stabilizes EF    .40 Stress Test Not low risk Follow on Medical Rx Evaluate LV function EF < .40 Low risk Early medical management Immediate angiography Braunwald E, et al. 2002.  http://www.acc.org/clinical/guidelines/unstable/unstable.pdf . Ongoing Evaluation in an Early Conservative Strategy
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 Follow on Medical Rx Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf ACC/AHA Guidelines for Unstable Angina and Non-ST-Segment Elevation MI Acute Ischemia Pathway   Early invasive strategy Early conservative strategy 12-24 hour  angiography Patient stabilizes EF  >  .40 Stress Test
Braunwald E, et al. Circ. 2002;106:1893. *  Recurrent ischemia; Trop;  ST; LV  failure/dysf.;  hemodynamic instability; VT; prior CABG     Enoxeparin. Preferred to UFH (IIa)    If coronary arteriography >24 hours ACC/AHA REVISED GUIDELINES UA/NSTEMI High Risk  * ASA, Heparin/ Enox. ,      block., Nitrates, Clopidogrel    RISK STRATIFY Low Risk
Braunwald E, et al. Circ. 2002;106:1893. ACC/AHA REVISED GUIDELINES LMCD, 3VD+LV Dys.,  or Diab. Mell. CABG High Risk Cor. Arteriography 1 or 2VD, Suitable  for PCI Normal Clopidogrel,  IIb/IIIa inhib. Consider Alternative  Diagnosis Discharge on ASA, Clopidogrel, Statin, ACEI PCI
Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf 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 I IIa IIb III
Tachydysrhythmias Regular Irregular Narrow   complex Wide complex Narrow complex Wide complex Sinus Tachycardia Atrial Tachycardia Atrial Flutter AVNRT/AVRT Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB MAT Atrial Fibrillation Atrial Flutter with  variable block Torsade des Pointes Ventricular fibrillation
Afib
Incidence of Afib
Risk Factors for Afib ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Morbidity of Afib in the ICU
Management ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Rate vs Rhythm control ,[object Object],[object Object],[object Object]
Chemical Cardioversion ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Chemical Cardioversion
Aflutter
SVT or Flutter? flutter
 
 
Vtach
Vfib
Vtach
Hyperkalemia
Hyperkalemia
Summary ,[object Object]

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Cardiogenic Shock And Arrhythmias

  • 1. Cardiogenic Shock, Acute Coronary Syndrome, Congestive Heart Failure, and Arrhythmias Dalhousie Critical Care Lecture Series
  • 2.
  • 3.
  • 4. 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 . Cardiogenic Shock
  • 5. Wall motion abnormality during occlusion Wall motion abnormality From Kloner RA. Am J Med. 1986;86:14. Gradual return of function (hours to days) Persistent wall motion abnormality (despite reperfusion and viable myocytes) Coronary occlusion Coronary reperfusion Return of function Clamp Schematic Diagram of Stunned Myocardium
  • 6. Cell death Significant residual stenosis Reperfusion Segments with myocardial stunning Segments with both stunning and hibernation Segments with hibernating myocardium Relief of ischemia Inotropic support No return of function Return of myocardial function Ischemic Myocardium
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12.
  • 13.
  • 14.
  • 16.
  • 17. Overall 30-Day Survival in the Study Hochman JS, et al. N Engl J Med. 1999;341:625-34. Proportion Alive 0 Days after Randomization 0.6 0.2 0.0 0.8 Revascularization (n =152) Medical therapy (n =150) 1.0 0.4 5 10 15 20 25 30 Survival = 53% Survival = 44% p = 0.11 Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock
  • 18. 46.7 50.3 54.3 56 63.1 66.4 0 20 40 60 80 100 % P = 0.11 P = 0.027 P < 0.03 30 days 6 months 1 year Revasc Med Rx SHOCK Trial Mortality
  • 19.
  • 20.
  • 21.
  • 22. Thus, excess nitric oxide and peroxy nitrites may be a major contributor to cardiogenic shock complicating MI. The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation.
  • 23.
  • 24. 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. Pathogenesis of Acute Coronary Syndromes
  • 25. UA/NSTEMI: Partially-occlusive thrombus (primarily platelets) Intra-plaque thrombus (platelet-dominated) Plaque core STEMI: Occlusive thrombus (platelets, red blood cells, and fibrin) Intra-plaque thrombus (platelet-dominated) Plaque core SUDDEN DEATH UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction Structure of Thrombus Following Plaque Disruption White HD. Am J Cardiol 1997;80 (4A):2B-10B.
  • 26. Therapeutic goal: rapidly break apart fibrin mesh to quickly restore blood flow ST-segment elevation MI Non-ST Elevation ACS* Non-ST Elevation MI + T roponin or + CK-MB Consider fibrinolytic therapy, if indicated, or primary percutaneous coronary intervention (PCI) Therapeutic goal: prevent progression to complete occlusion of coronary artery and resultant MI or death Consider GP IIb-IIIa inhibitor + aspirin + heparin before early diagnostic catheterization &/or Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf . Diagnostic Algorithm for Acute Coronary Syndrome Management
  • 27. 0 3 6 9 12 Probability of Death or MI Placebo Aspirin 75 mg Risk ratio 0.52 95% CL 0.37 - 0.72 Risk of MI and Death During Treatment with Low-Dose Aspirin and IV Heparin in Men with Unstable CAD Wallentin LC, et al. J Am Coll Cardiol, 1991;18:1587-93. Months 0.00 0.05 0.10 0.15 0.20 0.25
  • 28. Trial: FRIC (Dalteparin; n = 1,482) FRAXIS (nadroparin; n = 2,357) ESSENCE (enoxaparin; n = 3,171) TIMI 11B (enoxaparin; n = 3,910) .75 1.0 1.5     (p= 0.032) (p= 0.029) LMWH Better UFH Better 6 14 14 14 Day: Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf Low Molecular Weight Heparin (LMWH) vs. Unfractionated Haparin (UFH) in Non-ST elevation ACS: Effect on Death, MI, Recurrent Ischemia
  • 29. 0 2 4 6 8 10 12 14 Death, MI, or Stroke Clopidogrel + ASA 3 6 9 Placebo + ASA Months of Follow-Up 11.4% 9.3% 20% RRR P < 0.001 N = 12,562 0 12 % N Engl J Med. 2001;345:494-502. Effects of Clopidogrel in Addition to Aspirin in Patients with ACS without ST-Segment Elevation
  • 30. 15.7 5.6 17.9 11.7 12.8 14.2 3.8 12.9 10.3 11.8 0 5 10 15 20 Primary Endpoint % Placebo GP IIb/IIIa PURSUIT 30 days PRISM 48 hrs PRISM PLUS 7 days P = 0.04 P = 0.01 P = 0.004 PARAGON A 30 days P = 0.48 PARAGON B 30 days P = 0.33 Platelet Glycoprotein IIb/IIIa Inhibition for Non-ST elevation ACS Primary Endpoint Results from the 5 Major Trials
  • 31. 30 60 90 120 150 180 T-wave inversion 3.4% ST-segment elevation 6.8% ST-segment depression 8.9% Days from randomization % Cumulative Mortality at 6 Months Savonitto S. J Am Med Assoc. 1999; 281: 707-711. ST-segment Depression Predicts Higher Risk of Mortality in ACS 10% 8% 6% 4% 2%
  • 32.  
  • 33. Cannon. J Invas Cardiol. 2003;15:22B. Troponin and ST-Segment Shift Predict Benefit of Invasive Treatment Strategy
  • 34.
  • 35.
  • 36. Recurrent Symptoms/ischemia Heart failure Serious arrhythmia Patient stabilizes EF  .40 Stress Test Not low risk Follow on Medical Rx Evaluate LV function EF < .40 Low risk Early medical management Immediate angiography Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf . Ongoing Evaluation in an Early Conservative Strategy
  • 37. 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 Follow on Medical Rx Braunwald. Circulation. 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf ACC/AHA Guidelines for Unstable Angina and Non-ST-Segment Elevation MI Acute Ischemia Pathway Early invasive strategy Early conservative strategy 12-24 hour angiography Patient stabilizes EF > .40 Stress Test
  • 38. Braunwald E, et al. Circ. 2002;106:1893. * Recurrent ischemia; Trop; ST; LV failure/dysf.; hemodynamic instability; VT; prior CABG  Enoxeparin. Preferred to UFH (IIa)  If coronary arteriography >24 hours ACC/AHA REVISED GUIDELINES UA/NSTEMI High Risk * ASA, Heparin/ Enox. ,   block., Nitrates, Clopidogrel  RISK STRATIFY Low Risk
  • 39. Braunwald E, et al. Circ. 2002;106:1893. ACC/AHA REVISED GUIDELINES LMCD, 3VD+LV Dys., or Diab. Mell. CABG High Risk Cor. Arteriography 1 or 2VD, Suitable for PCI Normal Clopidogrel, IIb/IIIa inhib. Consider Alternative Diagnosis Discharge on ASA, Clopidogrel, Statin, ACEI PCI
  • 40. Braunwald. Circulation 2002;106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf 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 I IIa IIb III
  • 41. Tachydysrhythmias Regular Irregular Narrow complex Wide complex Narrow complex Wide complex Sinus Tachycardia Atrial Tachycardia Atrial Flutter AVNRT/AVRT Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB MAT Atrial Fibrillation Atrial Flutter with variable block Torsade des Pointes Ventricular fibrillation
  • 42. Afib
  • 44.
  • 45. Morbidity of Afib in the ICU
  • 46.
  • 47.
  • 48.
  • 49.
  • 51. SVT or Flutter? flutter
  • 52.  
  • 53.  
  • 54. Vtach
  • 55. Vfib
  • 56. Vtach
  • 59.