Management Cardiogenic Shock complicating AMIBagus Ari PradnyanaDepartment Cardiology & Vascular MedicineFaculty of Medicine Udayana University

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Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from cardiac dysfunction, most commonly following acute myocardial infarction (MI). The clinical definition of cardiogenic shock is

cardiac output (CO) and evidence of tissue hypoxia in the presence of adequate intravascular volume.Hemodynamic criteria for cardiogenic shock are

sustained hypotension (systolic blood pressure

Cardiogenic Shock, intracardiacMyocardial Injury or Obstruction to Flow

Arrythymiasvalvular lesionsAMISevere CHFVSDHypertrophic Cardiomyopathy

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Pathophysiology Myocardial Infarction

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Cardiogenic shock complicating AMIIncidence 7-25%Hospital Mortality

70s 90%20s 50%Indonesia ??

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Mortality : SHOCK registryJACC,2000 36(3): 1063

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ACC/AHA Guidelines Management STEMI 2004

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Management

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Cardiogenic Shock1-2 vessel CADModerate 3-vessel CADSevere 3-vessel CADLeft main CADPCI IRAPCI IRAImmediate CABGStaged Multivessel PCIStaged CABGCannot be performedEarly Shock, Diagnosed on Hospital PresentationDelayed Onset Shock Echocardiogram to Rule Out Mechanical DefectsCardiac Catheterization and Coronary AngiographyIABPFibrinolytic therapy if all of the following are present:

1.Greater than 90 minutes to PCI2.Less than 3 hours post STEMI onset3. No contraindications

Arrange prompt transfer to invasive procedure-capable centerArrange rapid transfer to invasive procedure-capable centerPCI for Cardiogenic Shock

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PCI After FibrinolysisIn patients whose anatomy is suitable, PCI should beperformed for the following:

Objective evidence of recurrent MI

Moderate or severe spontaneous/provocable myocardial ischemia during recovery from STEMI

Cardiogenic shock or hemodynamic instability.

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It is reasonable to perform primary PCI for patients with onset of symptoms within the prior 12 to 24 hours and 1 or more of the following:a. Severe CHFb. Hemodynamic or electrical instabilityc. Persistent ischemic symptoms.Primary PCI for STEMI:Specific Considerations

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Rescue PCIRescue PCI should be performed in patients less than 75 years old with ST elevation or LBBB who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.

Rescue PCI should be performed in patients with severe CHF and/or pulmonary edema (Killip class 3) and onset of symptoms within 12 hours.

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Rescue PCIRescue PCI is reasonable for selected patients 75 years or older with ST elevation or LBBB or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.

It is reasonable to perform rescue PCI for patients with one or more of the following:

a. Hemodynamic or electrical instability

b. Persistent ischemic symptoms.

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PCI for Cardiogenic ShockPrimary PCI is recommended for patients less than 75 years with ST elevation or LBBB or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock. Primary PCI is reasonable for selected patients 75 years or older with ST elevation or LBBB or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.

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Emergency Management of Complicated STEMIAdminister Fluids Blood transfusions Cause-specific interventions

Consider vasopressorsArrhythmiaBradycardiaTachycardiaSystolic BPGreater than 100 mm HgSystolic BP 70 to 100 mm HgNO signs/symptomsof shockSystolic BP70 to 100 mm HgSigns/symptomsof shockSystolic BP less than 70 mm Hg Signs/symptoms of shockDobutamine2 to 20 mcg/kg per minute IVLow Output -Cardiogenic Shock Nitroglycerin10 to 20 mcg/min IVDopamine5 to 15 mcg/kg per minute IVNorepinephrine0.5 to 30 mcg/min IVHypovolemiaAdminister Furosemide IV 0.5 to 1.0 mg/kg Morphine IV 2 to 4 mg Oxygen/intubation as needed Nitroglycerin SL, then 10 to 20 mcg/min IV if SBP greater than 100 mm Hg Dopamine 5 to 15 mcg/kg per minute IV if SBP 70 to 100 mm Hg and signs/symptoms of shock present Dobutamine 2 to 20 mcg/kg per minute IV if SBP 70 to 100 mm Hg and no signs/symptoms of shock

First line of actionSecond line of actionThird line of actionSee Section 7.7in the ACC/AHA Guidelines for Patients With ST-Elevation Myocardial InfarctionCheck Blood PressureClinical signs: Shock, hypoperfusion, congestive heart failure, acute pulmonary edemaMost likely major underlying disturbance?Further diagnostic/therapeutic considerations (should be considered in nonhypovolemic shock)Diagnostic Therapeutic Pulmonary artery catheter Intra-aortic balloon pump Echocardiography Reperfusion/revascularization Angiography for MI/ischemia Additional diagnostic studiesAcute Pulmonary EdemaCheck Blood PressureSystolic BP Greater than 100 mm Hg and not less than 30 mm Hg below baselineACE InhibitorsShort-acting agent such as captopril (1 to 6.25 mg)Circulation 2000;102(suppl I):I-172-I-216.

*The emergency management of patients with cardiogenic shock (CS), acute pulmonary edema (PE) or both is outlined.

Invasive monitoringBP monitoring

highly recommendedRight Heart catheterization

Supported by GUSTO-1SHOCK registryIakobishvili, Z, Med Clin N Am 91(2007) : 713-27

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Swan-Ganz Catheter

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Morphine and its analoguesIn patient present with restlessness and dyspnoea

Morphine induces Venodilatalion Mild arterial dilatation Reduce heart rate

Dose : 3 mg IV bolus Repeated if requiredESC guidelines Acute Heart Failure, 2005

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Diuretics For achieving optimal volume status eliminate or minimize congestion Progressive desaturation and pulmonary congestion CS need optimization of LV filling pressure to ensure maximal performance on starling force Might difficult : RHC, hourly monitored urine output

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ESC, Acute Heart Failure, 2005 Iakobishvili, Z, Med Clin N Am 91(2007) : 713-27

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Felker GM. Am Heart J. 2001;142:393401.

cardiogenic shock diuretic/ACE inhibitor refractory heart failure decompensationsa short-term bridge to definitive treatment, such as revascularization or cardiac transplantation, is potentially appropriate

Role of Inotropes

*Based on literature review of short- and long-term inotrope use in heart failure and national guidelines, recommendations can be made regarding the use of inotropes in heart failure.Available data suggest that long-term inotropic therapy has a negative impact on survival of patients with heart failure, regardless of the agent used. The data also suggest that short-term use in the hospital setting is associated with a significant increase in adverse events, no improvement in symptoms, increased risk of arrhythmias, and a trend for increased mortality. On the basis of the available evidence, the routine use of inotropes as heart failure therapy is not indicated in either the short- or long-term setting. Potentially appropriate uses of inotropes include as temporary treatment of refractory acute heart failure decompensations or as a bridge to definitive treatment, such as revascularization or cardiac transplantation; however, high-quality randomized evidence is lacking for the use of inotropes in these settings. Inotropes may also be appropriate as a palliative measure in patients with truly end-stage heart failure.1 Reference:Felker GM, OConnor CM. Inotropic therapy for heart failure: an evidence-based approach. Am Heart J. 2001;142:393401.

Sinus TachTreat cause; beta blockerAfib / FlutterTreat cause; slow ventricular rate; DC shock digoxin 0.125-0.25 mg IV or amiodaronePSVTVagal maneuvers; beta blocker, verapamil / diltiazem; DC shockArrhythmias During Acute Phase of STEMI: Pump Failure / Excess Sympathetic Tone ArrhythmiaTreatmentESC, Acute Heart Failure, 2005ACC/AHA Guidelines Management STEMI 2004

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Sinus BradyTreat if hemodynamic compromise;atropine / pacing

JunctionalTreat if hemodynamic compromise; atropine / pacing Arrhythmias During Acute Phase of STEMI: Bradyarrhythmias ArrhythmiaTreatmentACC/AHA Guidelines Management STEMI 2004

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SummaryAll resources must be used in Mechanical complication must be identified

May need different initial pharmacologic approachedIn the early stage shock it is essential to maintain MAP 60 mmhg with inotropic & IABPRevascularization is indicated for < 75 yo. within 18 hours of shock.PCI/CABG are preferred

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*The emergency management of patients with cardiogenic shock (CS), acute pulmonary edema (PE) or both is outlined. *

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*Based on literature review of short- and long-term inotrope use in heart failure and national guidelines, recommendations can be made regarding the use of inotropes in heart failure.Available data suggest that long-term inotropic therapy has a negative impact on survival of patients with heart failure, regardless of the agent used. The data also suggest that short-term use in the hospital setting is associated with a significant increase in adverse events, no improvement in symptoms, increased risk of arrhythmias, and a trend for increased mortality. On the basis of the available evidence, the routine use of inotropes as heart failure therapy is not indicated in either the short- or long-term setting. Potentially appropriate uses of inotropes include as temporary treatment of refractory acute heart failure decompensations or as a bridge to definitive treatment, such as revascularization or cardiac transplantation; however, high-quality randomized evidence is lacking for the use of inotropes in these settings. Inotropes may also be appropriate as a palliative measure in patients with truly end-stage heart failure.1 Reference:Felker GM, OConnor CM. Inotropic therapy for heart failure: an evidence-based approach. Am Heart J. 2001;142:393401.

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