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Shock Presentation Transcript

  • 1. Shock Scott G. Sagraves, MD, FACS Assistant Professor Trauma & Surgical Critical Care Associate Director of Trauma UHS of Eastern Carolina
  • 2. Objectives • • • • Define & classify shock Outline management principles Discuss goals of fluid resuscitation Understand the concepts of oxygen supply and demand in managing shock. • Describe the physiologic effects of vasopressors and inotropic agents
  • 3. Goals • Review hemodynamic techniques in the ICU • Introduce the concept of the cardiac cycle • Review of the pulmonary artery catheter parameters • Utilize the presentation to analyze clinical cases and to feel comfortable with pa-c parameters.
  • 4. Shock: “A momentary pause in the act of death.” -John Collins Warren, 1800s
  • 5. Hypotension • In Adults: – systolic BP ≤ 90 mm Hg – mean arterial pressure ≤ 60 mm Hg   systolic BP > 40 mm Hg from the patient’s baseline pressure
  • 6. Definition SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand.
  • 7. “Hypoperfusion can be present in the absence of significant hypotension.” -fccs course
  • 8. Pathophysiology ATP + H2O ⇒ ADP + Pi + H+ + Energy Acidosis results from the accumulation of acid when during anaerobic metabolism the creation of ATP from ADP is slowed. H+ shift extracellularly and a metabolic acidosis develops
  • 9. Pathophysiology • ATP production fails, the Na+/K+ pump fails resulting in the inability to correct the cell electronic potential. • Cell swelling occurs leading to rupture and death. • Oxidative Phosphorylation stops & anaerobic metabolism begins leading to lactic acid production.
  • 10. Why Monitor? • Essential to understanding their disease • Describe the patient’s physiologic status • Facilitates diagnosis and treatment of shock
  • 11. History • 1960’s – low BP = shock; MSOF resulted after BP restored • 1970’s – Swan & Ganz - flow-directed catheter – thermistor → cardiac output • 1980’s – resuscitation based on oxygen delivery, consumption & oxygen transport balance.
  • 12. Pulmonary Artery Catheter
  • 13. Pulmonary Artery Catheter • INDICATIONS – volume status – cardiac status • COMPLICATIONS – technical – anatomic – physiologic
  • 14. PLACEMENT
  • 15. West’s Lung Zones • Zone I - PA > Pa > Pv • Zone II - Pa > PA > Pv • Zone III - Pa > Pv > PA • PA = alveolar
  • 16. Correct PA-C Position
  • 17. Standard Parameters • Measured – Blood pressure – Pulmonary A. pressure – Heart rate – Cardiac Output – Stroke volume – Wedge pressure – CVP • Calculated – – – – Mean BP Mean PAP Cardiac Index Stroke volume index – SVRI – LVSWI – BSA
  • 18. Why Index? • Body habitus and size is individual • Inter-patient variability does not allow “normal” ranges • “Indexing” to patient with BSA allows for reproducible standard
  • 19. Index Example PATIENT A • • • • 60 yo male 50 kg CO = 4.0 L/min BSA = 1.86 CI = 2.4 L/min/m2 PATIENT B • • • • 60 yo male 150 kg CO = 4.0 L/min BSA = 2.64 CI = 1.5 L/min/m2
  • 20. PA Insertion 20 15 10 5 RA = 5 0 RV = 22/4 PA 19/10 PAOP = 9
  • 21. CVP • • • • CVP of SVC at level of right atrium pre-load “assessment” normal 4 - 10 mm Hg limited value
  • 22. PAOP • End expiration • Reflection changes with positive pressure • Waveforms change ≈ every 20 cm
  • 23. Waveform Analysis • A wave - atrial systole • C wave - tricuspid valve closure @ ventricular systole • V wave - venous filling of right atrium
  • 24. Cardiac Cycle PVRI MPAP RVSWI pulmonary Right ventricle CVP PCWP Left ventricle systemic SVRI MAP LVSWI
  • 25. Hemodynamic Calculations Parameter Cardiac Index (CI) Normal 2.8 - 4.2 Stroke Volume Index (SVI) 30 - 65 Sys Vasc Resistance Index (SVRI) 1600 - 2400 Left Vent Stroke Work Index (LVSWI) 43 - 62
  • 26. Cardiac Index C.I. = HR x SVI SVI measures the amount of blood ejected by the ventricle with each cardiac contraction. Total blood flow = beats per minute x blood volume ejected per beat
  • 27. Vascular Resistance Index SYSTEMIC (SVRI) MAP - CVP CI x 80 ↑ SVR = vasoconstriction ↓ SVR = vasodilation PULMONARY (PVRI) MPAP - PAOP CI x 80 ↑PVR = constriction PE, hypoxia Vascular resistance = change in pressure/blood flow
  • 28. Stroke Work LVSWI = (MAP-PAOP) x SVI x 0.0136 normal = 43 - 62 VSWI describe how well the ventricles are contracting and can be used to identify patients who have poor cardiac function. ventricular stroke work = ∆ pressure x vol. ejected
  • 29. Too Many Numbers
  • 30. Definitions • O2 Delivery - volume of gaseous O2 delivered to the LV/min. • O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min. • O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner Demand > consumption = anaerobic metabolism
  • 31. Rationale for Improving O2 Delivery Insult Tissue Hypoxia Demands are met Increased Delivery Increased Consumption
  • 32. VO2I Critical O2 Delivery The critical value is variable & is dependent upon the patient, disease, and the metabolic demands of the patient. DO2I
  • 33. Oxygen Calculations • Arterial Oxygen Content (CaO2) • Venous Oxygen Content (CvO2) • Arteriovenous Oxygen Difference (avDO2) • Delivery (O2AVI) • Consumption (VO2I) Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption
  • 34. Arterial Oxygen Content CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031) If low, check hemoglobin or pulmonary gas exchange
  • 35. Arteriovenous Oxygen Difference avDO2 = CaO2 - CvO2 Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock
  • 36. Oxygen Delivery (DO2I) O2AVI = CI x CaO2 x 10 Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues. < 400 is bad sign
  • 37. Oxygen Consumption VO2I = CI x (CaO2 - CvO2) If VO2I < 100 suggest tissues are not getting enough oxygen
  • 38. SvO2 SvO2 = 1- VO2 DO2
  • 39. Oxycalculations
  • 40. Resuscitation Goals • CI = 4.5 L/min/m2 • DO2I = 600 mL/min/m2 • VO2I = 170 mL/min/m2 NOT ALL PATIENTS CAN ACHIEVE THESE GOALS Critically ill patients who can respond to their disease states by spontaneously or artificially meeting these goals do show a better survival.
  • 41. Break Time…
  • 42. “Shock is a symptom of its cause.” -fccs course
  • 43. Signs of Organ Hypoperfusion • Mental Status Changes • Oliguria • Lactic Acidosis
  • 44. Components
  • 45. Categories of Shock • HYPOVOLEMIC • CARDIOGENIC • DISTRIBUTIVE • OBSTRUCTIVE
  • 46. Goals of Shock Resuscitation • Restore blood pressure • Normalize systemic perfusion • Preserve organ function
  • 47. In general, treat the cause...
  • 48. Hypovolemic Shock • Causes • Signs   cardiac – hemorrhage output – vomiting   PAOP – diarrhea   SVR – dehydration – third-space loss – burns
  • 49. Classes of Hypovolemic Shock
  • 50. Treatment - Hypovolemic • Reverse hypovolemia vs. hemorrhage control • Crystalloid vs. Colloid • PASG role? • Pressors?
  • 51. Resuscitation • Transport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial. • Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.
  • 52. Fluid Administration • • • • 1 L crystalloid ≈ 250 ml colloid crystalloids are cheaper blood must supplement either FFP for coagulopathy, NOT volume • Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused • NO survival benefit with colloids
  • 53. Role of PASG? • Houston - Higher mortality rate in penetrating thoracic, cardiac trauma • No benefit in penetrating cardiac trauma • Role undefined in rural, blunt trauma • Splinting role
  • 54. Cardiogenic Shock • Cause – defect in cardiac function • Signs      cardiac output  PAOP  SVR  left ventricular stroke work (LVSW)
  • 55. Coronary Perfusion Pressure Coronary PP = DBP - PAOP coronary perfusion = ∆ P across coronary a. GOAL - Coronary PP > 50 mm Hg
  • 56. The Failing Heart • Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient. • Fluids first, then cautious pressors • Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure) • If inotropes and vasopressors fail, intra-aortic balloon pump
  • 57. Distributive Shock • Types – – – – Sepsis Anaphylactic Acute adrenal insufficiency Neurogenic • Signs – ± cardiac output ± PAOP  SVR
  • 58. SIRS - Distributive Shock • Prompt volume replacement - fill the tank • Early antibiotic administration - treat the cause • Inotropes - first try Dopamine • If MAP < 60 – Dopamine = 2 - 3 µg/kg/min – Norepinephrine = titrate (1-100 µg/min) • R/O missed injury
  • 59. Adrenal Crisis Distributive Shock • Causes – Autoimmune adrenalitis – Adrenal apoplexy = B hemorrhage or infarct – heparin may predispose • Steroids may be lifesaving in the patient who is unresponsive to fluids, inotropic, and vasopressor support. Which one?
  • 60. Obstructive Shock • Causes – Cardiac Tamponade – Tension Pneumothorax – Massive Pulmonary Embolus • Signs   cardiac output   PAOP   SVR
  • 61. Endpoints? • ACS CoT ATLS - restoration of vital signs and evidence of end-organ perfusion • Swan-guided resuscitation – C.I. ≥ 4.5, DO2I ≥ 670, VO2I ≥ 166 • Lactic Acid clearance • Gastric pH
  • 62. Summary Type PAOP C.O. SVR HYPOVOLEMIC ↓ ↓ ↑ CARDIOGENIC ↑ ↓ ↑ DISTRIBUTIVE ↓ or N OBSTRUCTIVE ↑ varies ↓ ↓ ↑
  • 63. Vasopressor Agents? • Augments contractility, after preload established, thus improving cardiac output. • Risk tachycardia and increased myocardial oxygen consumption if used too soon • Rationale, increased C.I. improves global perfusion
  • 64. Vasopressors & Inotropic Agents • Dopamine • Norepinephrine • Dobutamine • Epinephrine • Amrinone
  • 65. Dopamine • Low dose (0.5 - 2 µg/kg/min) = dopaminergic • Moderate dose (3-10 µg/kg/min) = β-effects • High dose (> 10 µg/kg/min) = α-effects • SIDE EFFECTS – tachycardia – > 20 µg/kg/min ∆ to norepinephrine
  • 66. Dobutamine ∀ β-agonist • 5 - 20 µg/kg/min • potent inotrope, variable chronotrope • caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension
  • 67. Norepinephrine • Potent α-adrenergic vasopressor • Some β-adrenergic, inotropic, chronotropic • Dose 1 - 100 µg/min • Unproven effect with low-dose dopamine to protect renal and mesenteric flow.
  • 68. Epinephrine ∀ α- and β-adrenergic effects • potent inotrope and chronotrope • dose 1 - 10 µg/min • increases myocardial oxygen consumption particularly in coronary heart disease
  • 69. Amrinone • Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects • increased cardiac stroke output without an increase in cardiac stroke work • most often added with dobutamine as a second agent • load dose = 0.75 -1.5 mg/kg → 5 - 10 µg/kg/min drip • main side-effect - thrombocytopenia
  • 70. Dilators - inotropes + inotropes Pressors
  • 71. Summary `pressors & inotropes dilator Labetalol +2 Ca blocker ACE inhibitor hydralazine nitroglycerine Nipride β-blocker - inotrope Dobutamine Milrinone/Amrinone β-dopamine + inotrope Isuprel Digoxin Calcium epinephrine α-dopamine pressor neosynephrine norepinephrine
  • 72. Case Studies
  • 73. GSW • 24 year old male victim of a shotgun blast to his right lower quadrant/groin at close range. • Hemodynamically unstable in the field and his right lower extremity was cool and pulseless upon arrival to the trauma resuscitation area.
  • 74. Shotgun Blast
  • 75. Post-op • Patient received 12 L crystalloid, 15 units of blood, 6 units of FFP, and 2 6 packs of platelets. • HR 130, BP 96/48, T 34.7° C • PAWP 8, CVP 6, CI 4.2, SVRI 2700, LVSWI 42. Diagnosis? Treatment?
  • 76. SHOCK/HYPOVOLEMIA • FLUIDS… FLUIDS… FLUIDS… • BLOOD & PRODUCTS TRANSFUSION • CORRECT – ACIDOSIS – COAGULOPATHY – HYPOTHERMIA
  • 77. MVC • 38 year old female restrained driver who was involved in a high speed MVC. • She sustained a pulmonary contusion and fractured pelvis.
  • 78. ICU Course • Intubated and monitored with PA-C • PCWP = 22, CI = 3.5, SVRI = 2400, LVSWI = 39.8 • HR = 120, BP = 110/56, SpO2 = 91, UOP = 25 cc/hr What do you think...
  • 79. HYPOVOLEMIA ADJUST YOUR WEDGE FOR THE PEEP
  • 80. Wedge Adjustment • Measured PAOP - ½ PEEP = “real PAOP” • PEEP = 28, therefore “real wedge” = 8
  • 81. Auto-Pedestrian Crash • Thrown from the rear bed of pick up truck during a MVC at 60 mph. • Hemodynamically unstable • Pain to palpation of the pelvis • Hematuria with Foley® insertion
  • 82. ICU Course • Pelvis “closed” • QID Dressings, intubated, PA-C inserted • PCWP = 20, CI = 5.2, SVRI = 280, LVSWI = 24.5, PEEP = 8 Diagnosis? Treatment?
  • 83. Sepsis • Fluids • Correct the cause • Antibiotics • Debridement • Vasopressors – Phenylephrine – Levophed
  • 84. Initial Resuscitation • • • • • CVP: 8- 12 mm Hg MAP ≥ 65 mm Hg UOP ≥ 0.5 cc/kg/hr Mixed venous Oxygen Sat ≥ 70% Consider: – Transfusion to Hgb ≥ 10 – Dobutamine up to 20 µg/kg/min
  • 85. Vasopressors • Assure adequate fluid volume • Administer via CVL • Do not use dopamine for renal protection • Requires arterial line placement • Vasopressin: – Refractory shock – Infusion rate 0.01 – 0.04 Units/min
  • 86. Steroid Use in Sepsis • Refractory shock 200-300 mg/day of hydrocortisone in divided doses for 7 days • ACTH test • Once septic shock resolves, taper dose • Add fludrocortisone 50 µg po q day
  • 87. Geriatric Trauma • 70 year old female • MVC while talking on her cell phone • ruptured diaphragm and spleen s/p OR • Intubated and PA-C
  • 88. ICU Course • PCWP = 28, CI = 1.8, SVRI = 3150, LVSWI = 20.7 Diagnosis? Treatment?
  • 89. Cardiogenic Shock • Preload augmentation - Consider Fluids • Contractility – dopamine – dobutamine – phosphodiesterase inhibitor • Afterload reduction – nitroglycerin – dobutamine
  • 90. Don’t forget... Shock: “rude unhinging of the machinery of life.” -Samuel D. Gross, 1872