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Cardiogenic shock
Cardiogenic shock
Cardiogenic shock
Cardiogenic shock
Cardiogenic shock
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Cardiogenic shock
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Cardiogenic shock

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  • 1. CARDIOGENIC SHOCK POST OP MANAGEMENT VIKAS KOHLI MD FAAP FACC HOD PEDIATRIC CARDIOLOGIST BLK CHILDRENS HEART INSTITUTE BLK SUPERSPECIALITY HOSPITAL
  • 2. SCOPE AND POTENTIAL OF THIS TALK • BASICS OF WHY WE USE WHICH INOTROPE • BASIS OF INOTROPES • CLINICAL SCENARIOS • NEWER INOTROPES • ROLE OF ECHO • NOT ABOUT VENTILATION OR ABOUT TEACHING YOU ECHO
  • 3. CARDIOGENIC SHOCK: DEFINITION • The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.
  • 4. MOST COMMON EXAMPLE: MYOCARDITIS, FULMINANT • 3 mo old baby; otherwise well; recd vaccination 5 days back; then had URI • Now presents with • Respiratory distress • Poor feeding • Incessant crying
  • 5. CASE 1: PHYSICAL EX • Peripheral pulses poor • Extremities cold • Tachycardic to 190 bpm • S3 gallop + • Cap refill 5 s • Monitor: Sinus Tachycardia • BP: 50/35mmHg
  • 6. CHEST XRAY
  • 7. ECHO
  • 8. TREATMENT • IV Axis: Central Line, A line • Labs: CBC, Urea/Cr, Na/K/Mg/Ca, Liver Enzymes • Troponin I, CPK & MB • Maintenance Fluids with/out K+ • Ventilation to take care of work of breathing
  • 9. TREATMENT • Meds: Improve Cardiac Output • To improve BP would you start Adrenaline ?
  • 10. INOTROPES: OR ONE OF THESE ? • Dopamine • Dobutamine • Milrinone • Digoxin
  • 11. TREATMENT • Child started on: • Dopamine & Dobutamine • Both 7.5 mcg/kg/min • Diuretics; • Continous Infusion Vs Boluses • Ist dose Bolus • Ann Pharmacother. 2006 Oct;40(10):1797-803. Epub 2006 Sep 5. Efficacy and safety of a furosemide continuous infusion following cardiac surgery. • Intensive Care Med. 2001 Apr;27(4):711-5. Continuous intravenous furosemide in haemodynamically unstable children after cardiac surgery.
  • 12. BALANCE OF INOTROPY & VAODILATATION • Inotropy: • Dopamine • Dobutamine • Milrinone • Vasodilatation • Milrinone • Dobutamine • If BP permits: go up on the Vasodilatation • If Urine O/P not good: need more Vasodil • If Extremities not warm; need more vasodil
  • 13. INOTROPES & VASODILATATION • Once max required effect (not dose) of Inotropy & Vasodilatation achieved • Once renal function has stabalised & urine o/p is good: • Next step is to extubate the patient • Cardiac Function improvement is not required for extubation • Cardiac Output improvement is essential
  • 14. ECHO ADMISSION & 3 DAYS LATER
  • 15. CLINICAL SCENARIO: DAY 4 ECHO • Function has not changed but child now has: • Come off ventilator • And Inotropes are being weaned • So, with same function: how come now child is better ? • SYSTEMIC VASCULAR RESISTANCE
  • 16. SYSTEMIC VASCULAR RESISTANCE • Modulation of SVR changes Cardiac output • Previously SVR was very high • Now SVR has been brought down • So, Cardiac function has not changed but • Cardiac output has been increased
  • 17. FINAL STEPS • Getting them on oral medications • Inotropes: Digoxin • Diuretics: oral furosemide • Vasodilatation: Enalapril
  • 18. LONGTERM OUTCOME
  • 19. FULMINANT: CO MORBIDITIES • RENAL FAILURE • DIALYSIS • MENINGITIS • SEV HEPATIC DYSFUNCTION (Liver enzymes > 500) • VENTILATION • DURATION • MSOD
  • 20. FULMINANT: CO MORBIDITIES • ARRHYTHMIA • SUPRAVENTRICULAR • VENTRICULAR
  • 21. HOW GOOD DOES IT GET
  • 22. HOW GOOD DOES IT GET
  • 23. SUPPORTIVE MEDICATIONS • Carnitine 100 mg/kg • Thiamine (Benalgis) • CoEnzyme Q10 • All of unproven benefit
  • 24. NESIRITIDE
  • 25. NEWER DRUGS Pleconaril represents a promising new drug candidate for potential use in the treatment of human enteroviral infections.
  • 26. MYOCARDITIS AND VACCINATION • HISTORY NOTED • UNRELATED TO VACCINATION, BUT
  • 27. MYOCARDITIS AND VACCINATION • Methyl mercury enhanced the immune damage and chronicity of coxsackie B3 myocarditis in mice, compared with mice infected without prior mercury exposure • Ilback NG., Wesslen L., Fohlman Friman G. Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (Coxsackie B3 myocarditis) Toxicol. Lett. 1996;89:19-28 22.
  • 28. PERSONAL EXPERIENCE: MYOCARDITIS • Pancreatitis • Complete heart Block
  • 29. BETA BLOCKERS IN HEART FAILURE • substantial reductions in sudden death and death • Prevent progressive heart failure in patients • MERIT & CIBIS II trials • NYHA class II and III symptoms treated with blockers
  • 30. CARVEDILOL • Advisable to consider blockers in IDC patients with mild to moderate symptoms in spite of maximal treatment with ACE inhibitors • The Pediatric Randomized Carvedilol Trial in Children with Heart Failure • American College of Cardiology 55th Annual Scientific Session; March 11-14, 2006; Atlanta, Georgia. Smaller Trial Late-Breaking Clinical Trials II. Abstract 418-6.
  • 31. SPIRONOLACTONE • moderate to severe heart failure and contribute to sodium retention, potassium loss, sympathetic activation, myocardial fibrosis, and baroreceptor dysfunction • major source of aldosterone is reduced hepatic clearance rather than angiotensin dependent adrenal secretion
  • 32. SPIRONOLACTONE • with an ejection fraction < 35% and a history of NYHA class IV heart failure is associated with a 30% reduction in the overall risk of death RALES
  • 33. NESIRITIDE • ANP is released from atrial myocytes in response to stretch, and induces diuresis, naturesis, vasodilatation, and suppression of the renin-angiotensin system • ANP and brain natriuretic peptide are potent vasodilators and diuretics
  • 34. Levosimendan for low cardiac output: a pediatric experience. Egan JR, et al J Intensive Care Med 2006 July Levosimendan was safely used in a small number of pediatric patients with established low cardiac output state who demonstrated improved hemodynamics and tissue perfusion, with a tendency to reduced conventional inotrope usage, and this warrants its evaluation as an inotrope in the pediatric population.
  • 35. LEVOSIMENDAN Novel cardioprotective inotrope
  • 36. Pharmacokinetics • clinical effects prolonged due to active metabolite OR-1896 • Half life- 80hrs • Potentiates hemodynamics after cessation of parent drug • Dosing as indicated by clinical experience- Loading dose of 6-24µg/kg followed by infusion of < 0.4µg/kg/h
  • 37. 1. Enhances myocardial contractility by sensitizing myofilaments to intracellular calcium - binds to troponin C, stabilizes calcium-bound conformation and prolongs the systolic actin-myosin interaction 2. Role of KATP channel activation MITOCHONDRIAL KATP channels (mKATP) -
  • 38. SARCOLEMMAL MEMBRANE KATP CHANNELS Activation: - potassium ion efflux and membrane hyperpolarisation - inhibit inward L-type calcium current, lower intracellular calcium current, » vasodilatation in arteries, arterioles and veins * acts as an vasodilator agent on systemic vasculature and microcirculation * Key role in maintaining basal tone of coronary vasculature
  • 39. EFFECT ON LUSITROPHY • Diastolic dysfunction –major component of heart failure, present in up to 50% patients • Levosimendan does not appear to worsen lusitrophy due to its stabilizing action of the calcium-troponin C complex (and not increasing the binding affinity of calcium to troponin C)
  • 40. CARDIOVASCULAR EFFECTS OF LEVOSIMENDAN: Increase in -HR -CO -LV stroke volume Decrease in -LV EDP -SVR Also… • Increase blood flow to renal medulla & small intestine • Improved gastric mucosal oxygenation
  • 41. Unlike other positive inotropic agents (increase intracellular cAMP) - not associated with increased incidence of arrhythmias leading to cardiovascular mortality. ROLE IN ISCHAEMIA-REPERFUSION INJURY (during ischaemia, acidosis decreases calcium sensitivity in the failing heart) - levosimendan has potential to preserve contractile function (unique myofilament action)
  • 42. CLINICAL APPLICATIONS 1. HEART FAILURE- • beneficial effect on survival in acute decompensated failure compared to dobutamine at 31 and 108 days 2. INOPROTECTION- • positive inotropy +activation of KATP channels - cardiogenic shock - evolving myocardial infarction - perioperative ischaemia - emergence from CPB
  • 43. CONCLUSION • Judicious balance of • Preload • Myocardial fx • Afterload reduction • Tweaking the SVR may be the most important variable to change • Most patients can be managed without Extracorporeal support
  • 44. INOTROPY, CARDIAC OUTPUT, RENAL OUTPUT SECRET MANTRA TO IDEAL INOTROPY NIRVANA TO GREAT CARDIAC OUTPUT
  • 45. CARDIAC OUTPUT • PRELOAD • CARDIAC FUNCTION • AFTER LOAD • CARDIAC RHYTHM
  • 46. • Preload • Myocardial function • Afterload (systemic vascular resistance) • A combined or an individual effect of all these factors. • A decrease in preload, decrease in myocardial function and an increase in afterload allcause a decrease in renal perfusion. • The art is in assessing which of these is affecting the renal blood flow. Renal output is dependent on
  • 47. COMPENSATION, BP, MYOCARDIAL DYSFUNCTION • The myocardial function and SVR are clinically assessed by • the peripheral pulse being good and • the extremities being warm. • It is a misconception that myocardial function being poor would be reflected in the blood pressure of the child. • The body compensates for the decreased myocardial function (resulting in decreased cardiac output) by vasoconstriction (increase in SVR) and maintains the blood pressure. • At the cost of the splanchnic circulation (renal is part of it).
  • 48. PRELOAD • The preload is assessed by several mechanisms. One of the more reliable indicator in the ICU of the preload status is echocardiographic assessment of the IVC status. Serial assessment of respiratory variation and diameter of IVC are reliable indicators of fluid status of a child. • So, lack of respiratory variability and dilated IVC would indicate good or maximized preload status.
  • 49. PRELOAD Short of echocardiography, the most reliable clinical sign of assessing if improving the preload will bring down the heart rate and improve the BP is a gentle sustained pressure by hand on the liver. If the myocardium cannot handle the preload the pressure would go up temporarily only and heart rate would not come down but not come down. If the patient truly has occult or true volume depletion, the blood pressure would go up and heart rate come down. This response will be sustained till the hand is on the liver. This test must be performed with great caution in children with EF low
  • 50. AFTERLOAD REDUCTION • One has to be sure of lack of occult or true hypovolemia • If one is aware that the preload is adequate then one should initiate afterload reduction. • This is best achieved using Milrinone. • Dobutamine and Levosimendan are additional drugs which work in a similar fashion. • In cardiac patients, myocardial function is likely to be compromised if the patient is post op and inotropy without vasoconstriction should be used.
  • 51. CLINICAL THUMB RULES • 1. SVR is clinically assessed by the warmth of the extremity • 2. Cardiac output (a complex final endpoint of several factors) is assessed by • peripheral pulse volume. • 3. Need for Volume can be assessed by assessing serial IVC status • 4. Afterload reducing agents are heart friendly • 5. Vasoconstricting agents are not heart friendly (increase load on heart) • 6. Inotropes with vasodilating agents are best used because usually the etiology is multifactorial • 7. Prior to afterload reduction make sure occult hypovolemia is ruled out.
  • 52. PRELOAD • H/o blood loss • Excess urine output • Check clinically- • CVP • BP • Take help of ECHO • Correct accordingly
  • 53. MYOCARDIAL FUNCTION • Echocardiography • 4C view • Cross section view
  • 54. AFTERLOAD ASSESSMENT • Calculation of SVRI • Cardiac out put • Stroke volume
  • 55. RHYTHM ISSUE • Sinus tachycardia • JET • Supraventricular tachycardia • Atrial tachycardia • Bradycardia • Heart block
  • 56. Drugs Chrono Ionotro Vasodila Vasocon Dose mcg/kg/min Epi ++ + Low dose High dose 0.03-0.3 NorEpi + - - All dose 0.05-0.3 Dopa + + Low dose High dose Dobu - + Low dose High dose 0.5 to 5-10 Milrinone - + ++ - 0.03- 0.8
  • 57. CLINICAL CONDITIONS INTREPRETATION STEPS/DECISSION ↑ HR, poor pulse vol, cold limbs, ↑ CRT, ↓ urine, ↓ BP, ↑ Lactate LOW CO Start Ionotropic drugs- Dopa, Dobu Fluid bolius Elective ventilation ↑ HR, poor pulse vol cold limbs ↑ CRT, ↓ urine, Maintained BP ↑ Lactate LOW CO Add Diuretics Add ionodilators ↑ HR, Better pulse volume cold limbs ↑ CRT, Better urine output, BP-normal to high ↑ Lactate High after load Need MILRINONE
  • 58. ↑ HR, Good pulse vol warm limbs ↓ urine, BP- normal or lower side ↑ Lactate Relative hypovolemia Due to vasodilation Fluid challenge ↑ HR, Good pulse vol cold limbs ↓ urine BP- normal to high ↑ Lactate ↑ Afterload Milrinone ↑ HR, Low vol pulse cold limbs ↓ urine, ↓BP ↑ Lactate Hypovolemia Fluid boluses
  • 59. Setteled HR Good vol pulse Warm extremities Good urine Normal BP Normal lactate Optimized CO Maitain same ionotropes Plan weaning off the ventilator & extubation ↑HR Good vol pulse Warm extremities Decrease urine Normal BP ↑ Lacate Fall in CO Increase ionotropic support Setteled HR Good vol pulse Warm extremities Good urine Normal BP Normal lactate Optimum cardiac status Add oral ionotropes….taper intravenous ionotropes
  • 60. HOW TO TAPER IONOTROPES • Add Digoxin- slow digitalization • Once digitalization done- taper Dopamine by 0.1mcg/kg/min in every 1-2 hrs till reached 5 mcg/kg/min. Patient to be monitored • Clinically • by ABG, specifically by LACTATE. • Then taper Dobutamine same way upto 5 mcg/kg/min.
  • 61. HOW TO TAPER IONOTROPES • Once Dopamine and Dobutamine reached 5 mcg/kg/min add oral vasodilators- ENALAPRIL – give test dose 0.1mg/kg, look for • Hypotension • Effect of occult hypovolemia • Increase in serum urea • Decrease in urine out put. • Milrinone reduced to 1/2 dose after first test dose and if no hypotension, no increase in urea and no drop in urine output give 2nd dose. • If hemodynamics stable then taper dopa and dobuta gradually alternately. • Patient to be monitored by serum lactate level
  • 62. RHYTHM AS THE 4TH DIMENSION AFFECTING CARDIAC OUTPUT
  • 63. ARRHYTHMIA
  • 64. NORMAL SINUS RHYTHM Rate, rhythm, p wave, PR interval,QRS Rhythm generated by SA Node
  • 65. ECG
  • 66. NORMAL SINUS RHYTHM
  • 67. SINUS BRADYCARDIA… Normal in athletes', during sleep, drugs (beta blocker)
  • 68. SINUS TACHYCARDIA… Exercise, fever, anxiety, hypoxia, hypovolemia, low cardiac output
  • 69. SINUS ARRHYTHMIA Pacing rate of SAN varies with respiration
  • 70. SINUS ARRHYTHMIA
  • 71. SINUS RHYTHM • A A A A A • V V V V
  • 72. HOW DO BLOCKED PAC’S HAPPEN S S S S COMPENSATED PAUSE PAC
  • 73. SVT REENTRANT TACHYCARDIA • ATRIAL RATE HIGH; VENTRICULAR RATE SAME • A A A A A • V V V V V
  • 74. HOW DO BLOCKED PAC’S HAPPEN S S S S S S COMPENSATED PAUSE PAC
  • 75. HOW DOES BLOCKED PAC’S SIMULATE CHB • PAC’S A A A A A
  • 76. VENTRICULAR TACHYCARDIA A REMAINS NORMAL, V IS VERY HIGH RATE V V V V V V V V V
  • 77. PREMATURE ATRIAL CONTRACTION
  • 78. PAC WITH COMPENSATORY PAUSE
  • 79. ATRIAL TACHYCARDIA… Normal upright P but differ in shape from sinus p wave
  • 80. AF
  • 81. AF WITH COMPLETE HB
  • 82. AF WITH LAD
  • 83. BIGEMINY
  • 84. BIGEMINY
  • 85. COUPLETS
  • 86. SALVOS
  • 87. TDP; DC SHOCK; SINUS
  • 88. TDP PVC
  • 89. VT; VFIB
  • 90. TORSADE DE POINTES (TDP)
  • 91. PVC… From irritable ventricular focus. uniform or multiform PVC followed by full compensatory sinus pause P wave not associated with PVC, no relation with PR Wide bizarre QRS
  • 92. PVC UNIFORM…
  • 93. PVC MULTIFORM…
  • 94. PVC VENTRICULAR BIGEMINY…
  • 95. PVC VENTRICULAR TRIGEMINY…
  • 96. PVC QUADRIGEMINY…
  • 97. PVC COUPLETS…
  • 98. COUPLET
  • 99. PVC….R ON T PHENOMENON PVC occur so early to fall on T wave PVC occur during refractory period More vulnerable
  • 100. VERY RAPID RATE : SINUS VS SVT
  • 101. NARROW COMPLEX
  • 102. SVT
  • 103. VERY RAPID SVT
  • 104. ADENOSINE: PHARMACOLOGICAL CARDIOVERSION
  • 105. AVNRT NOW SINUS
  • 106. WPW
  • 107. WPW
  • 108. WPW
  • 109. AF
  • 110. AF W 2:1
  • 111. VT
  • 112. VT ? AF W ACCESORY PATHWAY
  • 113. VT VS SVT
  • 114. BIGEMINY
  • 115. BIGEMINY
  • 116. COUPLETS
  • 117. SALVOS
  • 118. TDP; DC SHOCK; SINUS
  • 119. TDP PVC
  • 120. VT; VFIB
  • 121. TORSADE DE POINTES (TDP)
  • 122. VT VS SVT
  • 123. WIDE COMPLEX TACHY
  • 124. WIDE COMPLEX VT
  • 125. TRACK THE P IN LAST LEAD
  • 126. AF WITH SLOW VENTR RESPONSE
  • 127. AF WITH RAPID VENTRICULAR RESPONSE
  • 128. WIDE COMPLEX TACHY
  • 129. YOUR OPINION
  • 130. JUNCTIONAL
  • 131. 12 YR OLD BOY HX PALPITATION
  • 132. SEARCHING FOR P WAVES GIVES THE ANSWER
  • 133. PACEMAKER
  • 134. HI K
  • 135. ELECTRICAL ALTERNANS
  • 136. JET
  • 137. JUNCTIONAL RHYTHM WITH RECIPROCAL P WAVE
  • 138. CONCLUSION • USE CLINICAL JUDGEMENT • ASSESS PRELOAD, MYOCARDIAL FX • AFTERLOAD • CLINICALLY • USE ECHO • DECIDE TO USE HEART FRIENDLY INOTROPES

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