Cardiogenic Shock And Arrhythmias
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Cardiogenic Shock And Arrhythmias Cardiogenic Shock And Arrhythmias Presentation Transcript

  • Cardiogenic Shock, Acute Coronary Syndrome, Congestive Heart Failure, and Arrhythmias Dalhousie Critical Care Lecture Series
    • 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/m 2 , PCWP > 15 mm Hg
    Parrillo, J. 2005 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
    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
    • 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
        • - Dobutamine
        • - Milrinone
    Initial Approach: Management
  • Dopamine
    • Dopaminergic, Beta, Alpha: ranges ?
    • Dopa: 1-5 ug/kg/min
      • ? Renal flow
    • Beta: 5-10 ug/kg/min
      • Inoptropy/chronotropy
    • Alpha: >10 ug/kg/min
      • Vasoconstriction
    • Major use: increasing HR, ?bp
  • Dobutamine
    • Beta (little alpha)
    • Inotropic/chronotropic
    • 2-20 ug/kg/min
    • Major use: Systolic dysfunction
    • Caveat: can/will decrease MAP
    • Often used in conjunction with levophed
  • Epinepherine
    • Alpha and Beta
    • 0.01 – 1.0 ug/kg/min
    • Major Use: when you need A&B
    • Like using dobutamine and levophed mixed together
  • Milrinone
    • Used as an inotrope
    • Mechanism of Action
      • Phosphodiesterase inhibitor
      • decrease the rate of cyclic AMP degradation
      • increase in cyclic AMP concentration leads to enhanced calcium influx into the cell, a rise in cell calcium concentration, and increased contractility
    • Side Effects
      • can also cause vasodilatation but tends to have less chronotropy than dobutamine
    • Onset of action
      • 5-15 minutes
    • Duration
      • Half life of approximately 2 hours (so its gonna last a while
    • Dose
      • Loading dose: 50 mcg/kg administered over 10 minutes followed by 0.375 mcg/kg/minute
  • Norepinepherine
    • Alpha and Beta
    • 0.02-3.0 ug/kg/min
    • Major Use: when you need A&B
      • ? Drug of choice for septic shock
      • Good and bad for use in cardiogenic shock
        • May increase blood pressure
        • May decrease CO by increasing afterload
        • Will increase cardiac strain
  • Use of Inotropes
    • BP is not a reliable indicator of CO
      • CO = SV X HR
      • MAP=SVR X CO
      • if SVR is increased as CO drops then MAP will stay the same
    • Need to titrate to the CO
      • Swan ganz CO measure
      • U/O
      • Lactate
      • ScVO2
  • Use of Vasopressors
    • Often used in conjunction with inotropes
      • counteract the vasodilation that occurs
    • Titrated to MAP
  • Intra-aortic Balloon Counterpulsation
    • The only thing that 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 as a bridge to definitive therapy
    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
    • 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)
    ACC/AHA Class I Indication
    • 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. Pathophysiology of Cardiogenic Shock Observations from the SHOCK Trial and Registry that Challenge the Classic Paradigm
    • 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 .
    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.
    • 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)
    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
    • Class I
    • An early invasive strategy in patients with a high-risk indicator:
    • 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 if not high risk
    ACC/AHA Guideline Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation MI
    • Start immediate
    • Aspirin
    • Heparin or low-molecular-weight heparin
    • GP IIb-IIIa inhibitor
    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
    • 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
    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
    • MICU
    • Electrolyte abnormalities
    • High cardiac filling pressures
    • Hypoxia
    • Comorbid heart disease
    • Sepsis
    • MOF
    • SICU
    • Post-op hypotension
    • Post-op sepsis
    • Post-op pulmonary edema
    • PA catheters
    • Blunt thoracic trauma
  • Morbidity of Afib in the ICU
  • Management
    • Stable vs. Unstable
      • Unstable
        • Electrical, synchronized cardioversion
        • 100J
      • Stable
        • Rate vs rhythm control
          • Rate control
            • Digoxin
            • B blocker
            • Verapamil
          • Rhythm control
            • Diltiazam
            • Amiodarone
            • magnesium
  • Rate vs Rhythm control
    • In non ICU patients rate vs rhythm control seems to make no difference
    • In the ICU patients may not tolerate lose of the atrial kick (up to 25% reduction in CO)
    • Most patients with new onset afib in the ICU will require a trial of chemical cardioversion
  • Chemical Cardioversion
    • Amiodarone
      • 300 mg bolus, then 1 g over 24 hr infusion
      • 75% will convert in 24 hrs
      • 5% incidence of hypotension
    • Diltiazam
      • 25 mg bolus, 20 mg/h infusion
      • 70% conversion
      • 30% hypotension
    • Magnesium
      • 86% conversion rate
      • No side effects
      • 37 mg/kg bolus followed by 25 mg/kg/hr for 24 hrs (approx 3 gm bolus then 2gm/hr for an 80kg patient)
    • Benign neglect
      • 56% cardioversion
    Chemical Cardioversion
  • Aflutter
  • SVT or Flutter? flutter
  •  
  •  
  • Vtach
  • Vfib
  • Vtach
  • Hyperkalemia
  • Hyperkalemia
  • Summary
    • Review ACLS guidelines