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Shock
- 1. Shock Scott G. Sagraves,MD, FACS Assistant Professor Trauma & Surgical Critical Care Associate Director of Trauma UHS of Eastern Carolina
- 2. Objectives • • • • Define & classifyshock 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 hemodynamictechniques 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 pausein 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 organperfusion to meet the tissue’s oxygenation demand.
- 7. “Hypoperfusion can be presentin 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 productionfails, 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? • Essentialto understanding their disease • Describe the patient’s physiologic status • Facilitates diagnosis and treatment of shock
- 11. History • 1960’s – lowBP = 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.
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- 13. Pulmonary Artery Catheter •INDICATIONS – volume status – cardiac status • COMPLICATIONS – technical – anatomic – physiologic
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- 15. West’s Lung Zones •Zone I - PA > Pa > Pv • Zone II - Pa > PA > Pv • Zone III - Pa > Pv > PA • PA = alveolar
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- 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? • Bodyhabitus 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 • • • • 60yo 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 SVCat 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 • Awave - 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 Leftventricle 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
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- 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 O2Delivery Insult Tissue Hypoxia Demands are met Increased Delivery Increased Consumption
- 32. VO2I Critical O2 Delivery Thecritical value is variable & is dependent upon the patient, disease, and the metabolic demands of the patient. DO2I
- 33. Oxygen Calculations • ArterialOxygen 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
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- 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.
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- 42. “Shock is asymptom of its cause.” -fccs course
- 43. Signs of Organ Hypoperfusion •Mental Status Changes • Oliguria • Lactic Acidosis
- 44.
- 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, treatthe cause...
- 48. Hypovolemic Shock • Causes •Signs cardiac – hemorrhage output – vomiting PAOP – diarrhea SVR – dehydration – third-space loss – burns
- 49.
- 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 Lcrystalloid ≈ 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 Acuteadrenal insufficiency Neurogenic • Signs – ± cardiac output ± PAOP SVR
- 58. SIRS - DistributiveShock • 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 CoTATLS - 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.
- 63. Vasopressor Agents? • Augmentscontractility, 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-adrenergicvasopressor • 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- andβ-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
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- 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
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- 73. GSW • 24 yearold 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.
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- 75. Post-op • Patient received12 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 yearold female restrained driver who was involved in a high speed MVC. • She sustained a pulmonary contusion and fractured pelvis.
- 78. ICU Course • Intubatedand 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 WEDGEFOR THE PEEP
- 80. Wedge Adjustment • MeasuredPAOP - ½ PEEP = “real PAOP” • PEEP = 28, therefore “real wedge” = 8
- 81. Auto-Pedestrian Crash • Thrownfrom 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
- 84. ICU Course • Pelvis“closed” • QID Dressings, intubated, PA-C inserted • PCWP = 20, CI = 5.2, SVRI = 280, LVSWI = 24.5, PEEP = 8 Diagnosis? Treatment?
- 85. Sepsis • Fluids • Correctthe cause • Antibiotics • Debridement • Vasopressors – Phenylephrine – Levophed
- 86. 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
- 87. Vasopressors • Assure adequatefluid 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
- 88. Steroid Use inSepsis • 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
- 89. Geriatric Trauma • 70year old female • MVC while talking on her cell phone • ruptured diaphragm and spleen s/p OR • Intubated and PA-C
- 90. ICU Course • PCWP= 28, CI = 1.8, SVRI = 3150, LVSWI = 20.7 Diagnosis? Treatment?
- 91. Cardiogenic Shock • Preloadaugmentation - Consider Fluids • Contractility – dopamine – dobutamine – phosphodiesterase inhibitor • Afterload reduction – nitroglycerin – dobutamine
- 92. Don’t forget... Shock: “rudeunhinging of the machinery of life.” -Samuel D. Gross, 1872