CARDIOGENIC SHOCK 2017 Eric Adler MD Associate Clinical Professor, UCSD

Transcription

1 CARDIOGENIC SHOCK 2017 Eric Adler MD Associate Clinical Professor, UCSD

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4 CARDIOGENIC SHOCK Definition INADEQUATE TISSUE PERFUSION RESULTING FROM CARDIAC DYSFUNCITON IN SETTING OF EUVOLEMIA HEMODYAMIC DEFINITION: SUSTAINED BP <90 for greater than 1 hour, CARDIAC INDEX <1.8 without inotropes, or 2.2 with inotropes AND PCWP >18.

5 Why Should I care about Cardiogenic Shock?? Up to 70% Mortality if not recognized. 100% of time on call person fellow and attending will be blamed if something bad happens. Prompt Interventions Are Lifesaving. Hentz fought the idea for days, snapping at family and nurses and shouting, "I hate you!" at one of her cardiologists, Dr. Eric Adler.

6 Incidence of Cardiogenic Shock Growing Cardiogenic Shock in STEMI Increasing 1 STEMI Cardiogenic Shock in Medicare Age Increasing 2 56,508 36,969 53% Dhaval Kolte et al. J Am Heart Assoc 2014 NATIONWIDE INPATIENT SAMPLE 2. Centers for Medicare and Medicaid database, MEDPAR FY14 Age >65 only, excludes non-medicare population

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8 Cardiogenic Shock Remains Leading Cause of Mortality in Acute Myocardial Infarction High In-Hospital Mortality During AMI Cardiogenic Shock 1 N = 23,696 and Ongoing Hazard Post Discharge after AMI Cardiogenic Shock 2 % N = 112,668 Death Rate, % Mortality % Post Discharge 1. Jeger, et al. Ann Intern Med Shah, et al. JACC 2016 NCDR Registry

9 HAVING SHOCK IS VERY BAD IABP (n=301) Medical Therapy (n=299)

10 High dose Vasopressors/inotropes Associated With Increased In-Hospital mortality Mortality Risk N = % 42% 2% 3% 7.5% 21% Three High Dose Samuels LE et al, J Card Surg. 1999

11 Pathophysiology of Disease

12 Cardiogenic Shock Etiology Acute myocardial infarction (most common cause) Occurs in 6-7% of acute MI Acute MR VSD Tamponade Myocarditis Hypertrophic Cardiomyopathy Arrhythmia

13 Evaluation of Patient in Cardiogenic Shock Tachycardic, SBP < 90, Narrow pulse pressure Cool extremities Altered mental status (obtunded, confused) S3 JVD/Edema/Rales EKG: Ischemia, Tamponade, Arrhythmia CXR: Cardiac Silhouette, Pneumothorax LABS: Decreased MVO2 Elevated Creatinine, BNP, LFTs, Lactate, Low Serum Sodium

14 Echocardiographic Findings in Cardiogenic Shock

15 Utility of MVO2

16 Using the Swan-Ganz catheter to diagnose type of shock

17 SHOCK PLAN DIAGNOSE IN TIMELY FASHION. DOCUMENT UNDERSTAND PATHOPHYSIOLGY ACT QUICKLY WORK TOGETHER NO ROOM FOR ERROR

18 Medical Therapy for Shock Volume Status Determine Volume Status: If CVP Low give fluid boluses (NS, Albumin, Blood) to keep CVP >8-10. If CVP >15 Initiate Diuresis. Bolus Diuretics (2X BUN given as IV Bolus of Lasix, or 2X outpatient oral dose given IV).

19 Vasodilation: Key element in Decompensated Heart Failure Management ADHF is a relatively vasoconstricted state Increased aldosterone, norepinephrine Results in elevated filling pressures and ultimately, congestion Vasoconstriction may lead to worsening mitral regurgitation (theoretical) Vasoconstriction may lead to purkinje fiber stretch and ultimately, arrhythmia (theoretical)

20 Supportive treatment Ø Inotropic agent : dopamine, dobutamine, milrinone, Vasopressors : norepinephrine,epinephrine, dopamine Ø IABP Ø Oxygen therapy and mechanical ventilator Ø Arrhythmia treatment Ø Magnesium, potassium, acidosis Ø Volume replacement for RV infarct ( L) or HOCM Ø Ventricular assist device (VAD) Ø Relief of pain and anxiety : morphine ( or fentanyl if SBP is compromised)

21 Inotropes and Vasopressors ACC/AHA Guidelines SBP <70:- Norepinephrine ( µg/min) Switch to Dopamine (5-15 µg/kg/min) once SBP 80 SBP Dopamine (5-15 µg/kg/min) Add dobutamine (2-20 µg/kg/min) once SBP 90

22 Reverse the Cardiogenic Shock Spiral MAP Cardiac Output Myocardial Recovery Patients End Organ Perfusion Cardiac Power Output Reverse Spiral Ischemia End Organ Failure Progressive Myocardial Dysfunction Death Spiral of Cardiogenic Shock

23 IABP- most common support for CS patients Stroke rate RISK: 1% 3% No IABP IABP BENEFIT: Meta-analysis of IABP in ST-elevation MI Sjauw et al., Eur Heart J (2009) IABP associated with only modest reduction in markers of disease severity Prondzinsky et al, Crit Care Med 2010

24 Hemodynamic Stabilization with Impella Unloads Left Ventricle & Coronary Perfusion End Organ Perfusion Right Side Support Escalation & Ambulation Right Side Impella RP Left Side Impella 2.5/CP/5.0 Seyfarth et al., JACC, 2008 Remmelink M et al., Cath Card Interv Lam K. et al,. Clin Res Cardiol, 2009 Casassus et a., JOIC, 2015 Anderson MB. et al., J Ht Lg Transplant Lima B. et al., Am J Cardiol 2016

25 Outflow (aortic root) Inflow (ventricle) Hemodynamic Effects of Impella aortic valve Support Flow MAP LVEDP and LVEDV Wall Tension Mechanical Work Coronary Perfusion Microvascular Resistance Cardiac Power Output End Organ Perfusion O 2 Supply O 2 Demand Unloading to Myocardial Recovery Fincke J, et al. Am Coll Cardiol 2004 Suga H. et al. Am J Physiol 1979 Sauren LDC, et al. Artif Organs 2007 Reesink KD, et al. Chest 2004 den Uil CA, et al. Eur Heart J 2010 Mendoza DD, et al. AMJ 2007 Torgersen C, et al. Crit Care 2009 Torre-Amione G, et al. J Card Fail 2009 Suga H, et al. Am J Physiol 1981 Burkhoff D. et al. Am J Physiol Heart Circ 2005 Burk hoff D. et al. Mechanic al Properties Of The Heart And Its Interac tion With The Vas c ular Sy s tem. (White Paper) 2011 Meyns B, et al. J Am Coll Cardiol 2003 Remmelink M, et al. atheter.cardiovasc Interv 2007 Aqel RA, et al. J Nucl Cardiol 2009 Lam K,. et al. Clin Res Cardiol 2009 Valgimigli M, et al.catheter Cardiovasc Interv 2005 Remmelink M. et al. Catheter Cardiovasc Interv 2010 Naidu S. et al. Novel Circulation.2011 Weber DM, et al. Cardiac Interventions Today Supplement Aug/Sep 2009

26 Improved Myocardial Perfusion with Impella Coronary Flow Velocity (cm/s) n=11 72 Impella OFF 61 18% p< Bedside planar images with gamma camera Impella ON Occluded RCA/LCX Territory Pre- Support On Support 1. Remmelink, et. al. CCI, Aqel et. al. J Nuclear Cardiology, 2009 CTO of LCX and RCA untreated 2

27 Crit Care Med Sep;38(9): Reduces LV preload Increases LV afterload Increased MO2 demand Impair myocardial protection ECMO No RCT 219 patients CS-MI treated with PCI 30 day survival in ECMO group 60% vs. 35% in historical non ECMO

28 Impella Unloading ECMO Patient Reduction in pulmonary congestion and LV dimension Jouan et al, J Hrt Lung Transplant, June 2009

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30 Time Management in CS Vasopressor and Inotropic support Short term improvement Increased O2 Demand If 2 required should place MCS Early Institution of MCS Before irreversible end-organ damage If intubation is required Type of device depends Presence of RV Dysfunction End Organ Dysfunction Goal MAP >60 mm Hg and a Mixed venous SO2 >70%

31 Patient presents on inotropes +/- IABP Algorithm to Support Cardiogenic Shock Within 2-3 hrs if CI not improved Unable to wean inotropes Requires moderate inotropes CI CPO W Short-term support Percutaneous partial support LVAD Hemodynamic instability with OMM Support Type Persistent decline Assisted CI<2 Assisted CPO < 0.6 W Continued inotropic dependence Requires high dose inotropes CI < 1.7 CPO < 0.53 W PCWP > 18 Respiratory distress Short-term support Percutaneous full support LVAD Inotropic dependence Anticipated support > 15 days Need for ambulation/discharge End organ dysfunction Known necrotic myocardium or irreversible process Large patient with type O blood group CPO < 0.53 W Impella 2.5 Impella 5.0 Recove ry Impella RP AB5000 RV Failure N o Weanin g Trial Unable to wean after 2 weeks support Pulsatile paracorporeal RVAD, LVAD, BiVAD Weaning Trial CVP > 18, low PCWP CI < 2.1 CPO < 0.6 W Acidosis not improving within 2 hrs No improvement in weaning trials > 2 months Tx Candidate? Transplant Durable VAD