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Post Operative Management

Dr.Mahmoud Abbas
Dr.Mahmoud Abbas
Dr.Mahmoud AbbasCEO Scribe of Egypt at Scribe of Egypt

Post Operative Management

1 of 55
Postoperative
            Management
            Jon N. Meliones, MD, MS, FCCM
                  Professor of Pediatrics
Medical Director Performance Improvement & Patient Safety
                  Medical Director PCICU
                      Duke University
Cardiogenic Shock
• Definition
  –Diagnosis
  –Effects of Shock
• Types of Shock
Oxygen Delivery
• Definition
  – Amount of oxygen being delivered to
    the tissues
  – DO2 = Oxygen Content x Cardiac
    Output
            DO2= CO * CaO2
 = (HR x SV) [(Hgb*1.36*SaO2) + (.003*PaO2)]
Determinants of Oxygen Delivery

      Preload
                 Stroke Volume
    Afterload
 Contractility
                               Cardiac Output
                  Heart Rate
                                         O2 DELIVERY

Hemoglobin (O2 capacity)
                               Oxygen Content
  Oxygen binding (SaO2)
Oxygen Dissolved (PaO2)
Pathophysiology of Shock




 O2 Supply < O2 Demand
Shock
• Definition
  – Inadequate DO2 to meet tissue needs
  – Cellular oxygen deficiency
  – Limitation or maldistribution of blood
    flow
• Compensated
• Uncompensated
• Irreversible
  – Organ failure & death
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Post Operative Management

  • 1. Postoperative Management Jon N. Meliones, MD, MS, FCCM Professor of Pediatrics Medical Director Performance Improvement & Patient Safety Medical Director PCICU Duke University
  • 2. Cardiogenic Shock • Definition –Diagnosis –Effects of Shock • Types of Shock
  • 3. Oxygen Delivery • Definition – Amount of oxygen being delivered to the tissues – DO2 = Oxygen Content x Cardiac Output DO2= CO * CaO2 = (HR x SV) [(Hgb*1.36*SaO2) + (.003*PaO2)]
  • 4. Determinants of Oxygen Delivery Preload Stroke Volume Afterload Contractility Cardiac Output Heart Rate O2 DELIVERY Hemoglobin (O2 capacity) Oxygen Content Oxygen binding (SaO2) Oxygen Dissolved (PaO2)
  • 5. Pathophysiology of Shock O2 Supply < O2 Demand
  • 6. Shock • Definition – Inadequate DO2 to meet tissue needs – Cellular oxygen deficiency – Limitation or maldistribution of blood flow • Compensated • Uncompensated • Irreversible – Organ failure & death
  • 7. LFTs, ileus ARDS MS SHOCK BP UO
  • 8. Shock: Diagnosis Noninvasive • Vital signs – HR, B.P. nl - ,  RR • End organ function –  UOP – Mental status changes – Liver dysfunction correlates with outcome
  • 9. Children’s Response BP= CO x SVR Heart rate Systemic Vascular % of Control Resistance 100 Blood Pressure Cardiac Output 25% 50% % Blood Volume Loss
  • 10. How to Measure CO? • CO = Heart Rate x Stroke Volume – SV determined by preload, afterload, contractility • Can we objective measure non- invasive measures of CO?
  • 11. Clinical Assessment of CO • Exam: – HR, BP, CVP – pulses – skin temperature, cap refill – UOP – Mental status
  • 12. Clinical Assessment of CO Surgeons Tibby, SM “Clinicians’ abilities to estimate cardiac index in ventilated children and infants” Arch Dis Child 1997
  • 13. Clinical Assessment of CO • Capillary Refill – May be useful marker of hypovolemia and myocardial function – ? Correlates with CO and lactate – Easy but… many confounding factors: fever, room temp, vasoactive drugs… careful! • Core vs peripheral temp. difference – >3 degrees associated with low output
  • 14. Central vs Peripheral Temp Metabolic Work Sweat Amount Core Temp Mahmoud Hero Hero Hero Mahmoud Mahmoud
  • 17. Defining Low Cardiac output Analysis of Arterial Wave Form D D P P Dt Dt • Upstroke – (Change Pressure (Dp)/(Change Time (Dt)) – Rapid = Good systolic function – Area under curve = stroke volume – FREE!!!!
  • 18. Defining Low Cardiac output • Metabolic Markers • Base deficit & pH –Easy to obtain –Poor correlation with outcome –Many confounders –Limitation - late
  • 19. Metabolic Markers • Lactate!!!! – Elevation (> 2.0) indicates inadequate tissue oxygen delivery – Initial Lactate < 7, Maximum < 9, 4-6 hr lactate < 4 predicts good outcome in post-op CHD (Duke, Boston, CHOP) – Rising Lactate = Bad outcome • Lactate change > 0.75 / hr = poor outcome
  • 20. Mixed Venous Saturations Amount of oxygen returning to heart (NL > 65%) Pulm Veins Vena Cava LA RA 70 99 70 99 LV RV 70 99 PA AO Lactate = NL
  • 21. Markers of O2 Delivery • Mixed Venous saturation – Fall in SVO2 may precede rise in lactate – Ideally sampled from PA • Rarely occurs in Pediatrics • SVC not too bad as reflects CNS – Central vein may be adequate for trends
  • 22. Low Mixed Venous Saturations Inadequate Oxygen delivery (More oxygen extracted by tissues) Pulm Veins Vena Cava LA RA 50 99 50 99 LV RV 50 99 PA AO Lactate = High
  • 23. High Mixed Venous Saturations Inadequate Oxygen Extraction (Tissues do not “see” oxygen) Pulm Veins Vena Cava LA RA 90 99 90 99 LV RV Great CO but, AO Lactate = High 90 99 PA
  • 24. Mixed Venous Saturations Lactates Mixed Lactate Intervent Venous Normal Normal None Low (DO2 High Inc. CO Low) Inc. CaO2 High (CO NL) High ????
  • 25. Markers of O2 Delivery • DO2 = VO2 x (arterio-venous difference) • AVO2 Difference – SaO2/ (SaO2 - SvO2) – Ex. .95/(.95 - .75)= 4.75 – Ex. .95/(.95 - .55)= 2.38 – Ex. .95/(.95 - .35)= 1.58 – Ex. .80/(.80 - .65)= 5.3 – Ex. .75/(.75 - .35)= 1.88
  • 26. Markers of O2 Delivery • Oxygen Extraction ratio – (SaO2 - SvO2) / SaO2 – Ex. (.95 - .75)/.95 = .20 • 20% of arterial oxygen is extracted – Ex. (.95 - .55)/.95 = .42 = 42% – Ex. (.80 - .65)/.80 = .19 = 19% – Ex. (.75 - .35)/.75 = .53 = 53% – Ratio <0.3 or < 30% indicative of adequate O2 delivery
  • 27. Defining Low Cardiac Output • Adequate Oxygen Delivery • O2 extraction < 0.3 • Lactate < 2.0 • Mixed venous –PvO2 > 28 –SVO2 > 60
  • 28. Defining Low Cardiac Output • Marginal Oxygen Delivery • O2 extraction 0.3 - 0.6 • Lactate < 2.0 • Mixed venous –PvO2 > 28 –SVO2 > 55
  • 29. Defining Low Cardiac Output • Inadequate Oxygen Delivery • O2 extraction >0.6 • Lactate >2.0 • Mixed venous –PvO2 < 28 –SVO2 < 55
  • 30. Cardiogenic Shock: Stagnant Hypoxia:  C.O. • C.O. = Heart Rate x Stroke Volume • Bradycardia  C.O. • Tachycardias  C.O. by  SV • Alterations in Stroke Volume
  • 31. Effects of Preload • Preload is a major determinant of DO2 • Preload augmentation has limitations (pressure effects may dominate) – When is volume too much…when  CVP with small infusion (Overdistention just like lung) – ed EDP may  CBF (especially  B.P.) –  ed Venous pressure •  ed LAP = Pulmonary edema •  ed CVP >15, Systemic edema
  • 32. Effects of Contractility •  Contractility directly  SV –  C.O. &  DO2 • Inotropic agents have varying effects • Neonatal myocardium – Ca++ strong inotrope – Less response to preload ( compliance) – Mature alpha receptors
  • 33. Effects of Afterload •  Afterload significantly  DO2 •  Afterload can dramatically  DO2 – Recent advancements Afterload reduction • Limitations of afterload reduction – CBF - Excessive vasodilation
  • 34. Neonatal vs Adult Heart • Limited responsiveness to inotropes –  Beta receptors & NE (?? Inotropes) – Less mature sympathetic system – Underdeveloped iCA regulatory mechanisms –  Muscle mass • Greater dependence of CO on HR and preload than contractility
  • 35. Myocardial Contraction • Contractility increases over 1st months of life along with: – #’s of sympathetic nerve fibers within myocardium – Total concentration of endogenous norepinephrine • There is a greater dependence of CO on HR than contractility during this time
  • 36. Low Cardiac Output Syndrome Decrease in CI in Newborns post ASO Wessel DL. Managing LCOS after CHD surgery. Crit Care Med 2001; 29:s220-230.
  • 37. Low Cardiac Output Syndrome
  • 38. Treatment for Systolic Dysfunction • Inotropic Agents:Improve Contractility • Ca++, Glucose, pH • Inotropes • PDEI • Vasodilators
  • 39. Inotropes • Dopamine myths • Epinephrine myths • What happened to Dobutamine? • Milrinone is it the answer?
  • 40. Low-Dose Dopamine: Renal Protective Effects. Effects on Renal Fx Markers* Criteria Dopamine (n=161) Placebo (n-163) Diff. Peak SCr ( mMol/L ) 245 (144) 249 (147) NS Peak BUN, 20 (10) 23 (12) NS Change in SCr ( mMol/L ) 62 (107) 66 (108) NS Change in BUN 6 (8) 7 (9) NS # w/ SCr > 300 ( mMol/L ) 56 56 NS Need for dialysis, 35 40 NS Urine output (ml/hr) Baseline 37 (40) 50 (59) NS After 1 hour 71 (81) 72 (77) NS After 24 hour 96 (101) 92 (72) NS After 48 hour 99 (83) 109 (95) NS * Mean (SD) “Low dose DA did not confer any significant protection from Renal Dysfunction.” Renal dose Dopamine does not exist (Bellomo R - Lancet 2000 )
  • 41. Cardiac Output # # 900 # 800 700 C.O. 600 500 (L / min.) 400 300 200 100 0 Pre DA Pre DB Pre EP DA DB EP # = p < 0.05 vs. Pre drug Mcgovern PCCM 2002
  • 42. PVR # 1600 1400 # Rin 1200 # 1000 (d-s/cm) 800 600 400 200 0 Pre DA Pre DB Pre EP DA DB EP # = p < 0.05 vs. Pre EP
  • 43. Inotropes Dopamine:  < 7 mcg/kg/min  Highest correlation with JET Epinephrine:  Dose not increase PVR/SVR Dobutamine:  Yes! Early
  • 44. Milrinone Minimal ↑ HR ↑ CO Diastolic Relaxation Minimal ↑ in ↓ SVR O2 demand ↓ PVR
  • 45. Milrinone • PDE 3 inhibitor • Inotropic- dilator • Dosing: -1 • Initial bolus: 25 to 100 μgkg -1 -1 • Infusion: 0.25 to 1.00 μgkg min • Half Life : 2-3 hr • 80 % excreted unchanged
  • 46. Primacorp Study: Results – LCOS/Death Development of LCOS / Death in first 36 hours post-op. (n = 227) Hoffman et al - Circulation 2003;107:996.)
  • 47. Vasodilators • Classified by site of action • Venodilators: reduce preload - Nitroglycerin • Arteriolar dilators: reduce afterload Minoxidil and Hydralazine • Combined: act on both arterial and venous beds and reduce both pre- and afterload Sodium Nitroprusside (Nipride)
  • 48. Downloaded from: Drugs for the Heart (on 29 January 2006 10:14 PM) © 2005 Elsevier
  • 49. Downloaded from: Drugs for the Heart (on 29 January 2006 10:14 PM) © 2005 Elsevier
  • 50. Sodium Nitroprusside • Direct NO donor • Increases cGMP in Vascular Smooth Muscle • Balanced venous and arterial dilatation • Short duration of action of 1-2 min -1 -1 • Dose: 0.25- 10 μgkg min • Indication: • Perioperative HTN • Hypertensive Crisis
  • 51. Sodium Nitroprusside • Clinical Effects: • Potent rapidly acting arterial and venous dilator produces ↓↓↓SVR, ↓↓↓PVR and ↓↓↓ preload • Reflex Tachycardia • Coronary steal • Inhibition of hypoxic pulmonary vaso constriction promotes V/Q mismatch and Hypoxia
  • 52. Sodium Nitroprusside • Side Effects • Precipitous hypotension • MI due to ↓ coronary perfusion pressure • Tachyphylaxis • Cyanide Toxicity • Hypoxia
  • 53. NITROGLYCERINE • Direct acting vasodilator requiring specific thiol intermediates to generate NO • Venodilation > arteriodilation • Rapid onset • Infusion: 0.5- to 10 mcg/kg/min, usual dose 1-3 mcg/kg/min • ↓ Preload causes ↓LV wall tension, ↑subendocardial perfusion, ↓ myocardial O2 demand • Superior Pulm. Vasodilator as compared to SNP
  • 55. Pearls • Heart rate, Core temp! • Preload – Optimize… if small infusions of volume result in increases in CVP /LAP ...STOP! • Contractility – Calcium… important but bolusing is bad – Dopamine…No data but consider up to 7 – Dobutamine…used in many institutions – Epinephrine…Low < 0.1  PVR / SVR – Milrinone…start at .75 but be careful in ARF as accumulation will occur